Strain Name:

B6;C3Fe a/a-Csf1op/J

Stock Number:

000231

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Availability:

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Mice homozygous for the osteopetrosis spontaneous mutation (Csf1op) may be useful to study the role of glia in neurological disease.

Description

Strain Information

Former Names B6C3Fe-a/a-Csf1op    (Changed: 15-JUL-09 )
B6C3Fe a/a-Csf1op/J    (Changed: 15-JUL-09 )
B6C3Fe-a/a-Csf1op    (Changed: 15-DEC-04 )
Type Mutant Stock; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHeterozygous x B6C3FeF1/J a/a Stock No. 001022
B6C3FeF1/J a/a Stock No. 001022 x Heterozygous
Specieslaboratory mouse
GenerationN66 (13-JAN-14)
Generation Definitions

Appearance
black, osteopetrosis
Related Genotype: a/a Csf1op/Csf1op

black, unaffected
Related Genotype: a/a Csf1op/+ or a/a ?/+

Description
Mice homozygous for the osteopetrosis spontaneous mutation (Csf1op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease.

Development
The osteopetrotic mutation arose spontaneously in 1970 at The Jackson Laboratory in the beginning congenic stock that became B6.DW-Pou1f1dw/J, which was then at generation N3. Osteopetrotic heterozygotes were backcrossed to C57BL/6J for 7 generations. The line was then bred once to C3FeLe.B6-a/a/J and the strain was subsequently maintained via homozygous ovarian transplant host bred to (C57BL/6J x C3FeLe.B6-a/a/J)F1 then intercross of the obligate heterozygous offspring.

Control Information

  Control
   Untyped from the colony
 
  Considerations for Choosing Controls

Related Strains

Alzheimer's Disease Models
005987   129-Achetm1Loc/J
006409   129S1.129(Cg)-Tg(APPSw)40Btla/Mmjax
008077   129S1/Sv-Bchetm1Loc/J
016198   129S6.Cg-Tg(Camk2a-tTA)1Mmay/JlwsJ
014556   129S6/SvEv-Apoetm4Mae/J
006555   A.129(B6)-Tg(APPSw)40Btla/Mmjax
005708   B6.129-Apbb1tm1Quhu/J
004714   B6.129-Bace1tm1Pcw/J
004098   B6.129-Klc1tm1Gsn/J
004193   B6.129-Psen1tm1Mpm/J
003615   B6.129-Psen1tm1Shn/J
005300   B6.129-Tg(APPSw)40Btla/Mmjax
005617   B6.129P-Psen2tm1Bdes/J
002609   B6.129P2-Nos2tm1Lau/J
007685   B6.129P2-Psen1tm1Vln/J
007999   B6.129P2-Sorl1Gt(Ex255)Byg/J
008087   B6.129S1-Bchetm1Loc/J
002509   B6.129S2-Plautm1Mlg/J
005301   B6.129S2-Tg(APP)8.9Btla/J
004163   B6.129S4-Cdk5r1tm1Lht/J
010959   B6.129S4-Grk5tm1Rjl/J
010960   B6.129S4-Grk5tm2Rjl/J
002213   B6.129S4-Ngfrtm1Jae/J
006406   B6.129S4-Tg(APPSwLon)96Btla/Mmjax
006469   B6.129S4-Tg(PSEN1H163R)G9Btla/J
012564   B6.129S5-Dhcr24tm1Lex/SbpaJ
004142   B6.129S7-Aplp2tm1Dbo/J
004133   B6.129S7-Apptm1Dbo/J
007251   B6.129X1-Mapttm1Hnd/J
013040   B6.Cg-Apoetm1Unc Ins2Akita/J
005642   B6.Cg-Clutm1Jakh/J
005491   B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
009126   B6.Cg-Nos2tm1Lau Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
005866   B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/Mmjax
008730   B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
005864   B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
007575   B6.Cg-Tg(CAG-Ngb,-EGFP)1Dgrn/J
016197   B6.Cg-Tg(CAG-OTC/CAT)4033Prab/J
005855   B6.Cg-Tg(Camk2a-Prkaca)426Tabe/J
007004   B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ
004996   B6.Cg-Tg(DBH-Gal)1923Stei/J
007673   B6.Cg-Tg(Gad1-EGFP)3Gfng/J
004662   B6.Cg-Tg(PDGFB-APP)5Lms/J
006293   B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2Mmjax
006006   B6.Cg-Tg(Prnp-APP)A-2Dbo/J
008596   B6.Cg-Tg(Prnp-Abca1)EHol/J
006005   B6.Cg-Tg(Prnp-App/APPswe)E1-2Dbo/Mmjax
007180   B6.Cg-Tg(Prnp-ITM2B/APP695*40)1Emcg/J
007182   B6.Cg-Tg(Prnp-ITM2B/APP695*42)A12Emcg/J
005999   B6.Cg-Tg(SBE/TK-luc)7Twc/J
012597   B6.Cg-Tg(Thy1-COL25A1)861Yfu/J
007051   B6.Cg-Tg(tetO-APPSwInd)102Dbo/Mmjax
007052   B6.Cg-Tg(tetO-APPSwInd)107Dbo/Mmjax
007049   B6.Cg-Tg(tetO-APPSwInd)885Dbo/Mmjax
009337   B6.FVB-Tg(Prnp-RTN3)2Yanr/J
006394   B6;129-Apba2tm1Sud Apba3tm1Sud Apba1tm1Sud/J
008364   B6;129-Chattm1(cre/ERT)Nat/J
008476   B6;129-Ncstntm1Sud/J
004807   B6;129-Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Mmjax
007605   B6;129P-Psen1tm1Vln/J
005618   B6;129P2-Bace2tm1Bdes/J
008333   B6;129P2-Dldtm1Ptl/J
002596   B6;129P2-Nos2tm1Lau/J
003822   B6;129S-Psen1tm1Shn/J
012639   B6;129S4-Mapttm3(HDAC2)Jae/J
012869   B6;129S6-Apbb2tm1Her/J
006410   B6;129S6-Chattm2(cre)Lowl/J
005993   B6;129S6-Pcsk9tm1Jdh/J
008636   B6;C-Tg(Prnp-APP695*/EYFP)49Gsn/J
007002   B6;C3-Tg(Prnp-ITM2B/APP695*42)A12Emcg/Mmjax
008169   B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J
008850   B6;SJL-Tg(Mt1-LDLR)93-4Reh/AgnJ
003378   B6C3-Tg(APP695)3Dbo Tg(PSEN1)5Dbo/J
004462   B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
003741   B6D2-Tg(Prnp-MAPT)43Vle/J
016556   B6N.129-Ptpn5tm1Pjlo/J
018957   B6N.129S6(B6)-Chattm2(cre)Lowl/J
024841   B6N.Cg-Tg(Prnp-MAPT*P301S)PS19Vle/J
006554   B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
012621   C.129S(B6)-Chrna3tm1.1Hwrt/J
002328   C.129S2-Plautm1Mlg/J
003375   C3B6-Tg(APP695)3Dbo/Mmjax
005087   C57BL/6-Tg(Camk2a-IDE)1Selk/J
005086   C57BL/6-Tg(Camk2a-MME)3Selk/J
008833   C57BL/6-Tg(Camk2a-UBB)3413-1Fwvl/J
007027   C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
010800   C57BL/6-Tg(Thy1-PTGS2)300Kand/J
010703   C57BL/6-Tg(Thy1-PTGS2)303Kand/J
005706   C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J
006618   C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J
007677   CB6-Tg(Gad1-EGFP)G42Zjh/J
007072   CByJ.129P2(B6)-Nos2tm1Lau/J
006472   D2.129(B6)-Tg(APPSw)40Btla/Mmjax
007067   D2.129P2(B6)-Apoetm1Unc/J
013719   D2.Cg-Apoetm1Unc Ins2Akita/J
003718   FVB-Tg(GadGFP)45704Swn/J
013732   FVB-Tg(NPEPPS)1Skar/J
013156   FVB-Tg(tetO-CDK5R1*)1Vln/J
015815   FVB-Tg(tetO-MAPT*P301L)#Kha/JlwsJ
002329   FVB.129S2-Plautm1Mlg/J
003753   FVB/N-Tg(Eno2CDK5R1)1Jdm/J
006143   FVB/N-Tg(Thy1-cre)1Vln/J
008051   NOD.129P2(B6)-Ctsbtm1Jde/RclJ
008390   STOCK Apptm1Sud/J
012640   STOCK Hdac2tm1.2Rdp/J
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
004779   STOCK Mapttm1(EGFP)Klt/J
014092   STOCK Tg(ACTB-tTA2,-MAPT/lacZ)1Luo/J
014544   STOCK Tg(tetO-ABL1*P242E*P249E)CPdav/J
View Alzheimer's Disease Models     (109 strains)

Parkinson's Disease Models
005987   129-Achetm1Loc/J
007587   129S-Park2tm1Rpa/J
002779   129S-Parp1tm1Zqw/J
017001   129S.B6N-Plk2tm1Elan/J
016198   129S6.Cg-Tg(Camk2a-tTA)1Mmay/JlwsJ
004608   B6(Cg)-Htra2mnd2/J
021828   B6(SJL)-Lrrk2tm3.1Mjff/J
008133   B6.129-Sncbtm1Sud/J
008084   B6.129P2-Drd4tm1Dkg/J
004744   B6.129P2-Esr1tm1Ksk/J
013586   B6.129P2-Gt(ROSA)26Sortm1Nik/J
002609   B6.129P2-Nos2tm1Lau/J
008843   B6.129P2-Sncgtm1Vlb/J
016566   B6.129S-Hcn1tm2Kndl/J
004322   B6.129S1-Mapk10tm1Flv/J
003190   B6.129S2-Drd2tm1Low/J
006582   B6.129S4-Park2tm1Shn/J
017946   B6.129S4-Pink1tm1Shn/J
005934   B6.129S4-Ucp2tm1Lowl/J
004936   B6.129S6(Cg)-Spp1tm1Blh/J
012453   B6.129X1(FVB)-Lrrk2tm1.1Cai/J
017009   B6.129X1-Nfe2l2tm1Ywk/J
009346   B6.Cg-Lrrk2tm1.1Shn/J
005491   B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
006577   B6.Cg-Park7tm1Shn/J
000567   B6.Cg-T2J +/+ Qkqk-v/J
007004   B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ
003139   B6.Cg-Tg(DBHn-lacZ)8Rpk/J
007673   B6.Cg-Tg(Gad1-EGFP)3Gfng/J
012466   B6.Cg-Tg(Lrrk2)6Yue/J
012467   B6.Cg-Tg(Lrrk2*G2019S)2Yue/J
008323   B6.Cg-Tg(Mc4r-MAPT/Sapphire)21Rck/J
008321   B6.Cg-Tg(Npy-MAPT/Sapphire)1Rck/J
008324   B6.Cg-Tg(Pmch-MAPT/CFP)1Rck/J
008322   B6.Cg-Tg(Pomc-MAPT/Topaz)1Rck/J
007894   B6.Cg-Tg(Rgs4-EGFP)4Lvt/J
012588   B6.Cg-Tg(TH-ALPP)1Erav/J
012265   B6.Cg-Tg(THY1-SNCA*A30P)TS2Sud/J
008859   B6.Cg-Tg(THY1-SNCA*A53T)F53Sud/J
008135   B6.Cg-Tg(THY1-SNCA*A53T)M53Sud/J
008601   B6.Cg-Tg(Th-cre)1Tmd/J
013583   B6.Cg-Tg(tetO-LRRK2)C7874Cai/J
000544   B6.D2-Cacna1atg/J
012445   B6.FVB-Tg(LRRK2)WT1Mjfa/J
012446   B6.FVB-Tg(LRRK2*G2019S)1Mjfa/J
006660   B6.SJL-Slc6a3tm1.1(cre)Bkmn/J
008364   B6;129-Chattm1(cre/ERT)Nat/J
009688   B6;129-Dbhtm2(Th)Rpa Thtm1Rpa/J
008883   B6;129-Gt(ROSA)26Sortm1(SNCA*A53T)Djmo/TmdJ
008889   B6;129-Gt(ROSA)26Sortm2(SNCA*119)Djmo/TmdJ
008886   B6;129-Gt(ROSA)26Sortm3(SNCA*E46K)Djmo/TmdJ
009347   B6;129-Lrrk2tm1.1Shn/J
016209   B6;129-Lrrk2tm2.1Shn/J
016210   B6;129-Lrrk2tm3.1Shn/J
013050   B6;129-Pink1tm1Aub/J
004807   B6;129-Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Mmjax
006390   B6;129-Sncatm1Sud Sncbtm1.1Sud/J
008532   B6;129-Thtm1(cre/Esr1)Nat/J
008333   B6;129P2-Dldtm1Ptl/J
008333   B6;129P2-Dldtm1Ptl/J
002596   B6;129P2-Nos2tm1Lau/J
003243   B6;129S-Tnfrsf1atm1Imx Tnfrsf1btm1Imx/J
003692   B6;129X1-Sncatm1Rosl/J
016575   B6;C3-Tg(PDGFB-LRRK2*G2019S)340Djmo/J
016576   B6;C3-Tg(PDGFB-LRRK2*R1441C)574Djmo/J
008169   B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J
004479   B6;C3-Tg(Prnp-SNCA*A53T)83Vle/J
012450   B6;D2-Tg(tetO-SNCA)1Cai/J
013725   B6;SJL-Tg(LRRK2)66Mjff/J
008473   B6;SJL-Tg(THY1-SNCA*A30P)M30Sud/J
008134   B6;SJL-Tg(THY1-SNCA*A30P)TS2Sud/J
016976   B6C3-Tg(tetO-SNCA*A53T)33Vle/J
000506   B6C3Fe a/a-Qkqk-v/J
003741   B6D2-Tg(Prnp-MAPT)43Vle/J
024841   B6N.Cg-Tg(Prnp-MAPT*P301S)PS19Vle/J
018768   B6N.Cg-Tg(SNCA*E46K)3Elan/J
012621   C.129S(B6)-Chrna3tm1.1Hwrt/J
016120   C57BL/6-Lrrk1tm1.1Mjff/J
012444   C57BL/6-Lrrk2tm1Mjfa/J
008389   C57BL/6-Tg(THY1-SNCA)1Sud/J
012769   C57BL/6-Tg(Thy1-Sncg)HvP36Putt/J
005706   C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J
006618   C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J
018785   C57BL/6J-Tg(LRRK2*G2019S)2AMjff/J
018786   C57BL/6J-Tg(LRRK2*R1441G)3IMjff/J
008245   C57BL/6J-Tg(Th-SNCA)5Eric/J
008239   C57BL/6J-Tg(Th-SNCA*A30P*A53T)39Eric/J
016122   C57BL/6N-Lrrk1tm1.1Mjff Lrrk2tm1.1Mjff/J
016121   C57BL/6N-Lrrk2tm1.1Mjff/J
016123   C57BL/6N-Sncatm1Mjff/J
016936   C57BL/6N-Tg(Thy1-SNCA)12Mjff/J
017682   C57BL/6N-Tg(Thy1-SNCA)15Mjff/J
007677   CB6-Tg(Gad1-EGFP)G42Zjh/J
009610   FVB/N-Tg(LRRK2)1Cjli/J
009609   FVB/N-Tg(LRRK2*G2019S)1Cjli/J
009604   FVB/N-Tg(LRRK2*R1441G)135Cjli/J
009090   FVB/NJ-Tg(Slc6a3-PARK2*Q311X)AXwy/J
017678   FVB;129-Pink1tm1Aub Tg(Prnp-SNCA*A53T)AAub/J
017744   FVB;129-Tg(Prnp-SNCA*A53T)AAub/J
010710   FVB;129S6-Sncatm1Nbm Tg(SNCA)1Nbm/J
010788   FVB;129S6-Sncatm1Nbm Tg(SNCA*A30P)1Nbm Tg(SNCA*A30P)2Nbm/J
010799   FVB;129S6-Sncatm1Nbm Tg(SNCA*A53T)1Nbm Tg(SNCA*A53T)2Nbm/J
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
000942   STOCK Pitx3ak/2J
014092   STOCK Tg(ACTB-tTA2,-MAPT/lacZ)1Luo/J
006340   STOCK Tg(Gad1-EGFP)98Agmo/J
017000   STOCK Tg(SNCA*E46K)3Elan/J
008474   STOCK Tg(THY1-SNCA*A53T)F53Sud/J
008132   STOCK Tg(THY1-Snca)M1mSud/J
012441   STOCK Tg(tetO-LRRK2*G2019S)E3Cai/J
012442   STOCK Tg(tetO-SNCA*A53T)E2Cai/J
012449   STOCK Tg(teto-LRRK2)C7874Cai/J
View Parkinson's Disease Models     (112 strains)

Strains carrying   a allele
003879   B10;TFLe-a/a T Itpr3tf/+ Itpr3tf/J
001538   B6 x B6C3Sn a/A-T(1;9)27H/J
000916   B6 x B6C3Sn a/A-T(5;12)31H/J
000602   B6 x B6C3Sn a/A-T(8;16)17H/J
000618   B6 x FSB/GnEi a/a Ctslfs/J
000577   B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J
000601   B6 x STOCK a/a T(7;18)50H/J
000592   B6 x STOCK T(2;4)13H a/J
014608   B6;129S1-a Kitlsl-24J/GrsrJ
000785   B6;D2-a Ces1ce/EiJ
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
001750   B6C3Fe a/a-Eif3cXs-J/J
002807   B6C3Fe a/a-Meox2fla/J
000506   B6C3Fe a/a-Qkqk-v/J
000224   B6C3Fe a/a-Scyl1mdf/J
003020   B6C3Fe a/a-Zdhhc21dep/J
001037   B6C3Fe a/a-Agtpbp1pcd/J
000221   B6C3Fe a/a-Alx4lst-J/J
002062   B6C3Fe a/a-Atp7aMo-8J/J
001756   B6C3Fe a/a-Cacng2stg/J
001815   B6C3Fe a/a-Col1a2oim/J
000209   B6C3Fe a/a-Dh/J
000211   B6C3Fe a/a-Dstdt-J/J
000210   B6C3Fe a/a-Edardl-J/J
000207   B6C3Fe a/a-Edaraddcr/J
000182   B6C3Fe a/a-Eef1a2wst/J
001278   B6C3Fe a/a-Glra1spd/J
000241   B6C3Fe a/a-Glrbspa/J
002875   B6C3Fe a/a-Hoxd13spdh/J
000304   B6C3Fe a/a-Krt71Ca Scn8amed-J/J
000226   B6C3Fe a/a-Largemyd/J
000636   B6C3Fe a/a-Lmx1adr-J/J
001280   B6C3Fe a/a-Lse/J
001573   B6C3Fe a/a-MitfMi/J
001035   B6C3Fe a/a-Napahyh/J
000181   B6C3Fe a/a-Otogtwt/J
000278   B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J
000205   B6C3Fe a/a-Papss2bm/J
002078   B6C3Fe a/a-Pcdh15av-2J/J
000246   B6C3Fe a/a-Pitpnavb/J
001430   B6C3Fe a/a-Ptch1mes/J
000235   B6C3Fe a/a-Relnrl/J
000237   B6C3Fe a/a-Rorasg/J
000290   B6C3Fe a/a-Sox10Dom/J
000230   B6C3Fe a/a-Tcirg1oc/J
003612   B6C3Fe a/a-Trak1hyrt/J
001512   B6C3Fe a/a-Ttnmdm/J
001607   B6C3Fe a/a-Unc5crcm/J
000005   B6C3Fe a/a-Wc/J
000243   B6C3Fe a/a-Wnt1sw/J
000248   B6C3Fe a/a-Xpl/J
000624   B6C3Fe a/a-anx/J
008044   B6C3Fe a/a-bpck/J
002018   B6C3Fe a/a-din/J
002339   B6C3Fe a/a-nma/J
000240   B6C3Fe a/a-soc/J
000063   B6C3Fe a/a-sy/J
001055   B6C3Fe a/a-tip/J
000245   B6C3Fe a/a-tn/J
000296   B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J
000019   B6C3Fe-a/a-Itpr1opt/J
001022   B6C3FeF1/J a/a
006450   B6EiC3 a/A-Vss/GrsrJ
000971   B6EiC3 a/A-Och/J
000551   B6EiC3 a/A-Tbx15de-H/J
000557   B6EiC3-+ a/LnpUl A/J
000503   B6EiC3Sn a/A-Gy/J
001811   B6EiC3Sn a/A-Otcspf-ash/J
002343   B6EiC3Sn a/A-Otcspf/J
000391   B6EiC3Sn a/A-Pax6Sey-Dey/J
001923   B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J
000225   C3FeLe.B6 a/a-Ptpn6me/J
000198   C3FeLe.B6-a/J
000291   C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J
001886   C3HeB/FeJLe a/a-gnd/J
000584   C57BL/6J-+ T(1;2)5Ca/a +/J
000284   CWD/LeJ
000670   DBA/1J
000671   DBA/2J
001057   HPT/LeJ
000260   JGBF/LeJ
000265   MY/HuLeJ
000308   SSL/LeJ
000994   STOCK a Myo5ad Mregdsu/J
000064   STOCK a Tyrp1b Pmelsi/J
002238   STOCK a Tyrp1b shmy/J
001433   STOCK a skt/J
000579   STOCK a tp/J
000319   STOCK a us/J
002648   STOCK a/a Cln6nclf/J
000317   STOCK a/a Egfrwa2/J
000302   STOCK a/a MitfMi-wh +/+ Itpr1opt/J
000286   STOCK a/a Myo5ad fd/+ +/J
000206   STOCK a/a Tyrc-h/J
001432   STOCK a/a Tyrp1b Ndc1sks/Tyrp1b +/J
000281   STOCK a/a ma Flgft/J
000312   STOCK stb + a/+ Fignfi a/J
000596   STOCK T(2;11)30H/+ x AEJ-a Gdf5bp-H/J or A/J-a Gdf5bp-J/J
000970   STOCK T(2;16)28H A/T(2;16)28H a/J
000590   STOCK T(2;4)1Sn a/J
000594   STOCK T(2;8)26H a/T(2;8)26H a Tyrp1+/Tyrp1b/J
000623   TR/DiEiJ
View Strains carrying   a     (102 strains)

View Strains carrying other alleles of Csf1     (3 strains)

Strains carrying other alleles of a
002655   Mus pahari/EiJ
000251   AEJ.Cg-ae +/a Gdf5bp-H/J
000202   AEJ/Gn-bd/J
000199   AEJ/GnLeJ
000433   B10.C-H3c H13? A/(28NX)SnJ
000427   B10.CE-H13b Aw/(30NX)SnJ
000423   B10.KR-H13? A/SnJ
000420   B10.LP-H13b Aw/Sn
000477   B10.PA-Bloc1s6pa H3e at/SnJ
000419   B10.UW-H3b we Pax1un at/SnJ
000593   B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J
000502   B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J
000599   B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J
002083   B6 x B6EiC3 a/A-T(7;16)235Dn/J
000507   B6 x B6EiC3 a/A-Otcspf/J
003759   B6 x B6EiC3Sn a/A-T(10;16)232Dn/J
002071   B6 x B6EiC3Sn a/A-T(11;17)202Dn/J
002113   B6 x B6EiC3Sn a/A-T(11A2;16B3)238Dn/J
002068   B6 x B6EiC3Sn a/A-T(11B1;16B5)233Dn/J
002069   B6 x B6EiC3Sn a/A-T(14E4or5;16B5)225Dn/J
001926   B6 x B6EiC3Sn a/A-T(15;16)198Dn/J
001832   B6 x B6EiC3Sn a/A-T(15E;16B1)60Dn/J
003758   B6 x B6EiC3Sn a/A-T(16C3-4;17A2)65Dn/J
001833   B6 x B6EiC3Sn a/A-T(1C2;16C3)45Dn/J
001903   B6 x B6EiC3Sn a/A-T(6F;18C)57Dn/J
001535   B6 x B6EiC3Sn a/A-T(8A4;12D1)69Dn/J
001831   B6 x B6EiC3Sn a/A-T(8C3;16B5)164Dn/J
002016   B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ
000600   B6-Gpi1b x B6CBCa Aw-J/A-T(7;15)9H Gpi1a/J
000769   B6.C/(HZ18)By-at-44J/J
000203   B6.C3-Aiy/a/J
000017   B6.C3-Avy/J
001572   B6.C3-am-J/J
000628   B6.CE-A Amy1b Amy2a5b/J
001809   B6.Cg-Aw-J EdaTa-6J +/+ ArTfm/J
000552   B6.Cg-Aw-J EdaTa-6J Sxr
001730   B6.Cg-Aw-J EdaTa-6J Sxrb Hya-/J
000841   B6.Cg-Aw-J EdaTa-By/J
000021   B6.Cg-Ay/J
100409   B6129PF1/J-Aw-J/Aw
004200   B6;CBACa Aw-J/A-Npr2cn-2J/GrsrJ
000505   B6C3 Aw-J/A-Bloc1s5mu/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
000065   B6C3Fe a/a-we Pax1un at/J
003301   B6C3FeF1 a/A-Eya1bor/J
000314   B6CBACa Aw-J/A-EdaTa/J-XO
000501   B6CBACa Aw-J/A-Aifm1Hq/J
001046   B6CBACa Aw-J/A-Grid2Lc/J
000500   B6CBACa Aw-J/A-Gs/J
002703   B6CBACa Aw-J/A-Hydinhy3/J
000247   B6CBACa Aw-J/A-Kcnj6wv/J
000287   B6CBACa Aw-J/A-Plp1jp EdaTa/J
000515   B6CBACa Aw-J/A-SfnEr/J
000242   B6CBACa Aw-J/A-spc/J
000288   B6CBACa Aw-J/A-we a Mafbkr/J
001201   B6CBACaF1/J-Aw-J/A
006450   B6EiC3 a/A-Vss/GrsrJ
000557   B6EiC3-+ a/LnpUl A/J
000504   B6EiC3Sn a/A-Cacnb4lh/J
000553   B6EiC3Sn a/A-Egfrwa2 Wnt3avt/J
001811   B6EiC3Sn a/A-Otcspf-ash/J
002343   B6EiC3Sn a/A-Otcspf/J
001923   B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J
001875   B6EiC3SnF1/J
000638   C3FeB6 A/Aw-J-Sptbn4qv-J/J
000200   C3FeB6 A/Aw-J-Ankank/J
001203   C3FeB6F1/J A/Aw-J
001272   C3H/HeSnJ-Ahvy/J
000099   C3HeB/FeJ-Avy/J
000338   C57BL/6J Aw-J-EdaTa-6J/J
000258   C57BL/6J-Ai/a/J
000774   C57BL/6J-Asy/a/J
000569   C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J
000051   C57BL/6J-Aw-J/J
000055   C57BL/6J-at-33J/J
000070   C57BL/6J-atd/J
002468   KK.Cg-Ay/J
000262   LS/LeJ
000283   LT.CAST-A/J
001759   STOCK A Tyrc Sha/J
001427   STOCK Aw us/J
001145   WSB/EiJ
View Strains carrying other alleles of a     (82 strains)

Additional Web Information

Visit the Alzheimer's Disease Mouse Model Resource site for helpful information on Alzheimer's Disease and research resources.

Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Csf1op/Csf1op

        B6C3Fe a/a-Csf1op/J
  • mortality/aging
  • partial postnatal lethality
    • reduced numbers of homozygotes survive to weaning   (MGI Ref ID J:73663)
  • growth/size/body phenotype
  • decreased body weight   (MGI Ref ID J:104139)
    • low body weight   (MGI Ref ID J:73663)
  • postnatal growth retardation
    • slower growth rate   (MGI Ref ID J:73663)
  • immune system phenotype
  • abnormal Kupffer cell morphology
    • 30% fewer Kupffer cells than normal littermates   (MGI Ref ID J:26978)
    • irregular distribution of Kupffer cells in liver lobules   (MGI Ref ID J:26978)
    • Kupffer cells possess phagocytized blood cells, poorly developed organelles and microvilli projections   (MGI Ref ID J:26978)
  • abnormal Langerhans cell morphology
    • bone chimera experiments suggest hematopoietic precursors to Langerhans cells have reduced capability to differentiate into Langerhan cells when skin is inflammed   (MGI Ref ID J:112594)
    • absent Langerhans cell
      • absence of Langerhans cells in newborns but numbers recover in adults   (MGI Ref ID J:112594)
  • abnormal Langerhans cell physiology
    • Langerhan cell numbers are slow to recover after UV irradiation   (MGI Ref ID J:112594)
    • two weeks after UV irradiation, numbers are 25% compared to unirradiated mutant mice while at the same timepoint irradiated wild-type LC numbers are close to 100% of control   (MGI Ref ID J:112594)
  • abnormal microglial cell morphology
    • reduced numbers of microglial cells in frontal cortex, parietal cortex and corpus callosum   (MGI Ref ID J:49613)
    • microglial cells in frontal cortex have smaller cell bodies and shorter cytoplasmic processes   (MGI Ref ID J:49613)
  • abnormal osteoclast morphology
    • reduced size and number of multinuclear osteoclasts   (MGI Ref ID J:26978)
    • abnormal osteoclast differentiation
      • daily injection of exogenous M-CSF recruits functional osteoclasts   (MGI Ref ID J:4732)
      • minimally a single injection of 5 micrograms rhM-CSF is needed for transient recruitment of osteoclasts   (MGI Ref ID J:4732)
      • linked to impaired remodeling of bone and no marrow cavity formation in long bones   (MGI Ref ID J:19549)
  • abnormal perivascular macrophage morphology
    • reduced numbers of perivascular macrophages (as identified by F4/80 staining) are found in parietal cortex   (MGI Ref ID J:49613)
  • abnormal spleen red pulp morphology
    • extensive extramedullary hematopoiesis   (MGI Ref ID J:26978)
  • abnormal splenic cell ratio
    • increased concentration of CFU-S cells, however , size and differentiation pattern of spleen colonies is normal   (MGI Ref ID J:104139)
    • spleen mostly composed of fibroblastoid cells   (MGI Ref ID J:104139)
    • reduced number of macrophages   (MGI Ref ID J:104139)
  • abnormal splenocyte physiology
    • mutants have prolonged hemopoiesis   (MGI Ref ID J:19549)
  • abnormal thymus medulla morphology
    • atrophic with numerous macrophages   (MGI Ref ID J:26978)
  • decreased leukocyte cell number   (MGI Ref ID J:104139)
    • decreased macrophage cell number
      • decreased numbers of macrophages in liver, spleen, bone marrow, kidney, subcutaneous tissue, uterus and ovary   (MGI Ref ID J:26978)
      • macrophages exhibit intracytoplasmic organelles in splenic, thymic and bone marrow   (MGI Ref ID J:26978)
      • macrophage organelles and microvillous projections are poorly developed   (MGI Ref ID J:26978)
      • decreased numbers in spleen and marrow   (MGI Ref ID J:104139)
      • decreased osteoclast cell number
        • TRAP+ cells (osteoclasts) were present in low numbers in the bony trabecula regions compared to controls   (MGI Ref ID J:73663)
    • decreased monocyte cell number
      • almost complete absence of monocytes in peripheral blood   (MGI Ref ID J:104139)
  • thymus cortex hypoplasia
    • consists mostly of thymic epithelial cells   (MGI Ref ID J:26978)
  • skeleton phenotype
  • abnormal bone marrow cavity morphology
    • reduced numbers of hematopoietic cells   (MGI Ref ID J:26978)
    • none in long bones where no bone remodeling occurs   (MGI Ref ID J:19549)
    • apparent at postnatal Day 2 and by Day 7 femoral marrow cellularity and progenitor cell content was significantly reduced   (MGI Ref ID J:19549)
  • abnormal bone marrow morphology
    • femoral bone marrow cellularity is reduced early but recovers to control levels by 8 months of age   (MGI Ref ID J:73663)
  • abnormal bone remodeling
    • in long bones, therefore no marrow cavity formation   (MGI Ref ID J:19549)
  • abnormal femur morphology
    • distal end is wide, diaphysis does not have a well defined cortex   (MGI Ref ID J:18356)
  • abnormal long bone hypertrophic chondrocyte zone   (MGI Ref ID J:26978)
  • abnormal osteoclast morphology
    • reduced size and number of multinuclear osteoclasts   (MGI Ref ID J:26978)
    • abnormal osteoclast differentiation
      • daily injection of exogenous M-CSF recruits functional osteoclasts   (MGI Ref ID J:4732)
      • minimally a single injection of 5 micrograms rhM-CSF is needed for transient recruitment of osteoclasts   (MGI Ref ID J:4732)
      • linked to impaired remodeling of bone and no marrow cavity formation in long bones   (MGI Ref ID J:19549)
    • decreased osteoclast cell number
      • TRAP+ cells (osteoclasts) were present in low numbers in the bony trabecula regions compared to controls   (MGI Ref ID J:73663)
  • abnormal parietal bone morphology
    • parietal bone grows only through the trabecular bone formation with no subperiosteal bone lamellae forming as in normal mice   (MGI Ref ID J:18356)
  • abnormal tibia morphology
    • proximal end is wide, diaphysis does not have a well defined cortex   (MGI Ref ID J:26978)
  • domed cranium
    • flat bone grows without resorption while keeping the normal primary curvature resulting in a more globular skull   (MGI Ref ID J:18356)
  • increased bone trabecula number
    • higher amounts of bony trabeculae   (MGI Ref ID J:73663)
    • excessive amount of bone trabeculae   (MGI Ref ID J:26978)
  • reproductive system phenotype
  • abnormal mammary gland growth during pregnancy
    • lobulo-alveolar development is premature and occupies 56% of mammary gland by day 18 of pregnancy   (MGI Ref ID J:20519)
  • abnormal uterus development
    • poor development of glandular epithelia   (MGI Ref ID J:26978)
  • endometrium hypoplasia
    • endometrium is hypoplastic   (MGI Ref ID J:26978)
  • increased testis weight
    • as a percentage of body weight, testicular tissue is increased over controls   (MGI Ref ID J:34371)
  • myometrium hypoplasia
    • myometrium is hypoplastic   (MGI Ref ID J:26978)
  • necrospermia
    • percentage of dead sperm is two times higher than controls   (MGI Ref ID J:34371)
  • oligozoospermia
    • epididymal sperm count 60% lower than control   (MGI Ref ID J:34371)
  • reduced male fertility
    • males take 5 times longer to mate than controls   (MGI Ref ID J:34371)
    • males mate on the first night, but not on subsequent nights in timed mating experiments   (MGI Ref ID J:34371)
  • nervous system phenotype
  • abnormal microglial cell morphology
    • reduced numbers of microglial cells in frontal cortex, parietal cortex and corpus callosum   (MGI Ref ID J:49613)
    • microglial cells in frontal cortex have smaller cell bodies and shorter cytoplasmic processes   (MGI Ref ID J:49613)
  • amyloid beta deposits
    • 100 to 200 fibrillar plaques observed in cerebral cortex   (MGI Ref ID J:87261)
    • 20 to 60 plaques observed in amygdala and hypothalamus   (MGI Ref ID J:87261)
    • small number of plaques observed in hippocampus   (MGI Ref ID J:87261)
  • decreased hippocampus pyramidal cell number
    • hippocampal neuron loss in CA1 and CA3 regions   (MGI Ref ID J:87261)
  • hematopoietic system phenotype
  • abnormal Kupffer cell morphology
    • 30% fewer Kupffer cells than normal littermates   (MGI Ref ID J:26978)
    • irregular distribution of Kupffer cells in liver lobules   (MGI Ref ID J:26978)
    • Kupffer cells possess phagocytized blood cells, poorly developed organelles and microvilli projections   (MGI Ref ID J:26978)
  • abnormal Langerhans cell morphology
    • bone chimera experiments suggest hematopoietic precursors to Langerhans cells have reduced capability to differentiate into Langerhan cells when skin is inflammed   (MGI Ref ID J:112594)
    • absent Langerhans cell
      • absence of Langerhans cells in newborns but numbers recover in adults   (MGI Ref ID J:112594)
  • abnormal bone marrow cell morphology/development   (MGI Ref ID J:19549)
    • decreased bone marrow cell number
      • number of cells 10 fold less than controls   (MGI Ref ID J:104139)
      • marrow mostly composed of fibroblastoid cells   (MGI Ref ID J:104139)
      • reduced numbers of CFU-S cells   (MGI Ref ID J:104139)
  • abnormal hematopoietic stem cell morphology   (MGI Ref ID J:19549)
  • abnormal microglial cell morphology
    • reduced numbers of microglial cells in frontal cortex, parietal cortex and corpus callosum   (MGI Ref ID J:49613)
    • microglial cells in frontal cortex have smaller cell bodies and shorter cytoplasmic processes   (MGI Ref ID J:49613)
  • abnormal osteoclast morphology
    • reduced size and number of multinuclear osteoclasts   (MGI Ref ID J:26978)
    • abnormal osteoclast differentiation
      • daily injection of exogenous M-CSF recruits functional osteoclasts   (MGI Ref ID J:4732)
      • minimally a single injection of 5 micrograms rhM-CSF is needed for transient recruitment of osteoclasts   (MGI Ref ID J:4732)
      • linked to impaired remodeling of bone and no marrow cavity formation in long bones   (MGI Ref ID J:19549)
  • abnormal perivascular macrophage morphology
    • reduced numbers of perivascular macrophages (as identified by F4/80 staining) are found in parietal cortex   (MGI Ref ID J:49613)
  • abnormal spleen red pulp morphology
    • extensive extramedullary hematopoiesis   (MGI Ref ID J:26978)
  • abnormal splenic cell ratio
    • increased concentration of CFU-S cells, however , size and differentiation pattern of spleen colonies is normal   (MGI Ref ID J:104139)
    • spleen mostly composed of fibroblastoid cells   (MGI Ref ID J:104139)
    • reduced number of macrophages   (MGI Ref ID J:104139)
  • abnormal splenocyte physiology
    • mutants have prolonged hemopoiesis   (MGI Ref ID J:19549)
  • abnormal thymus medulla morphology
    • atrophic with numerous macrophages   (MGI Ref ID J:26978)
  • decreased leukocyte cell number   (MGI Ref ID J:104139)
    • decreased macrophage cell number
      • decreased numbers of macrophages in liver, spleen, bone marrow, kidney, subcutaneous tissue, uterus and ovary   (MGI Ref ID J:26978)
      • macrophages exhibit intracytoplasmic organelles in splenic, thymic and bone marrow   (MGI Ref ID J:26978)
      • macrophage organelles and microvillous projections are poorly developed   (MGI Ref ID J:26978)
      • decreased numbers in spleen and marrow   (MGI Ref ID J:104139)
      • decreased osteoclast cell number
        • TRAP+ cells (osteoclasts) were present in low numbers in the bony trabecula regions compared to controls   (MGI Ref ID J:73663)
    • decreased monocyte cell number
      • almost complete absence of monocytes in peripheral blood   (MGI Ref ID J:104139)
  • extramedullary hematopoiesis
    • observed in splenic red pulp   (MGI Ref ID J:26978)
  • thymus cortex hypoplasia
    • consists mostly of thymic epithelial cells   (MGI Ref ID J:26978)
  • liver/biliary system phenotype
  • abnormal Kupffer cell morphology
    • 30% fewer Kupffer cells than normal littermates   (MGI Ref ID J:26978)
    • irregular distribution of Kupffer cells in liver lobules   (MGI Ref ID J:26978)
    • Kupffer cells possess phagocytized blood cells, poorly developed organelles and microvilli projections   (MGI Ref ID J:26978)
  • limbs/digits/tail phenotype
  • abnormal femur morphology
    • distal end is wide, diaphysis does not have a well defined cortex   (MGI Ref ID J:18356)
  • abnormal tibia morphology
    • proximal end is wide, diaphysis does not have a well defined cortex   (MGI Ref ID J:26978)
  • endocrine/exocrine gland phenotype
  • abnormal lactation
    • only 10% of females can lactate, however, lactation in this subset is inefficient   (MGI Ref ID J:20519)
  • abnormal mammary gland development
    • postpartum females exhibit incompletely differentiated mammary gland tissue with a nonsecretory phenotype   (MGI Ref ID J:20519)
    • alveolar cells are cuboidal, contain large lipid vesicles and the lumen is small or unformed   (MGI Ref ID J:20519)
    • abnormal branching of the mammary ductal tree
      • ductal structures are poorly developed with incomplete arborization   (MGI Ref ID J:20519)
    • abnormal mammary gland growth during pregnancy
      • lobulo-alveolar development is premature and occupies 56% of mammary gland by day 18 of pregnancy   (MGI Ref ID J:20519)
  • increased testis weight
    • as a percentage of body weight, testicular tissue is increased over controls   (MGI Ref ID J:34371)
  • homeostasis/metabolism phenotype
  • decreased circulating testosterone level   (MGI Ref ID J:34371)
  • hearing/vestibular/ear phenotype
  • abnormal auditory brainstem response
    • delayed and diminished response to brainstem auditory evoked potential (BAEP)   (MGI Ref ID J:19549)
  • abnormal vestibular system physiology
    • poorly formed or absent response to surface visual evoked potential (VEP)   (MGI Ref ID J:19549)
  • other phenotype
  • amyloid beta deposits
    • 100 to 200 fibrillar plaques observed in cerebral cortex   (MGI Ref ID J:87261)
    • 20 to 60 plaques observed in amygdala and hypothalamus   (MGI Ref ID J:87261)
    • small number of plaques observed in hippocampus   (MGI Ref ID J:87261)
  • cardiovascular system phenotype
  • abnormal Kupffer cell morphology
    • 30% fewer Kupffer cells than normal littermates   (MGI Ref ID J:26978)
    • irregular distribution of Kupffer cells in liver lobules   (MGI Ref ID J:26978)
    • Kupffer cells possess phagocytized blood cells, poorly developed organelles and microvilli projections   (MGI Ref ID J:26978)
  • abnormal perivascular macrophage morphology
    • reduced numbers of perivascular macrophages (as identified by F4/80 staining) are found in parietal cortex   (MGI Ref ID J:49613)
  • craniofacial phenotype
  • abnormal parietal bone morphology
    • parietal bone grows only through the trabecular bone formation with no subperiosteal bone lamellae forming as in normal mice   (MGI Ref ID J:18356)
  • domed cranium
    • flat bone grows without resorption while keeping the normal primary curvature resulting in a more globular skull   (MGI Ref ID J:18356)
  • muscle phenotype
  • abnormal masseter muscle morphology
    • severely atrophied white and intermediate muscle fibers are observed in the superficial region of the masseter muscle   (MGI Ref ID J:20589)
    • the progression and extent of atrophy differed among regions of the muscle   (MGI Ref ID J:20589)
    • the decrease in diameter of muscle fibers was larger than found in mice fed a granulated diet   (MGI Ref ID J:20589)
    • the decrease in sensory input due to underdevelopment of periodontal ligaments in the absence of teeth likely results in atrophy of the masseter muscle   (MGI Ref ID J:20589)
  • vision/eye phenotype
  • abnormal visual evoked potential
    • total intracortical transmembrane current significantly reduced as measured by intracortical VEP   (MGI Ref ID J:19549)
    • altered neural firing as demonstrated by multiple unit activity (MUA) measurement   (MGI Ref ID J:19549)
  • integument phenotype
  • abnormal lactation
    • only 10% of females can lactate, however, lactation in this subset is inefficient   (MGI Ref ID J:20519)
  • abnormal mammary gland development
    • postpartum females exhibit incompletely differentiated mammary gland tissue with a nonsecretory phenotype   (MGI Ref ID J:20519)
    • alveolar cells are cuboidal, contain large lipid vesicles and the lumen is small or unformed   (MGI Ref ID J:20519)
    • abnormal branching of the mammary ductal tree
      • ductal structures are poorly developed with incomplete arborization   (MGI Ref ID J:20519)
    • abnormal mammary gland growth during pregnancy
      • lobulo-alveolar development is premature and occupies 56% of mammary gland by day 18 of pregnancy   (MGI Ref ID J:20519)
  • cellular phenotype
  • abnormal osteoclast differentiation
    • daily injection of exogenous M-CSF recruits functional osteoclasts   (MGI Ref ID J:4732)
    • minimally a single injection of 5 micrograms rhM-CSF is needed for transient recruitment of osteoclasts   (MGI Ref ID J:4732)
    • linked to impaired remodeling of bone and no marrow cavity formation in long bones   (MGI Ref ID J:19549)

Csf1op/Csf1op

        involves: C3HeB/FeJ * C57BL/6J
  • homeostasis/metabolism phenotype
  • abnormal circulating calcium level
    • unable to raise serum calcium concentration in response to parathyroid extract (PTE)   (MGI Ref ID J:5634)
  • decreased circulating phosphate level
    • phosphate serum levels are low but calcium levels are normal   (MGI Ref ID J:5634)
  • decreased circulating testosterone level
    • mutant male mice have a seven-fold lower concentration of circulating testosterone than wild-type mice   (MGI Ref ID J:34371)
  • behavior/neurological phenotype
  • abnormal eating behavior
    • pups drink less of the mother's milk possibly due to being unable to compete with normal littermates   (MGI Ref ID J:40136)
  • abnormal mating frequency
    • only 64.4% of superovulated mutant females successfully mated as evidenced by a vaginal plug compared with 88.9% of mated superovulated heterozygous females   (MGI Ref ID J:38039)
    • reduced male mating frequency
      • normal mating behavior is restored following treatment with circulating testosterone or CSF-1 throughout the postnatal period   (MGI Ref ID J:34371)
  • cardiovascular system phenotype
  • decreased susceptibility to atherosclerosis
    • mice on a high fat diet for 15 weeks develop smaller atherosclerosis lesions than do the C57BL/6J controls   (MGI Ref ID J:40136)
    • lesions are also less frequent and when present, less advanced with no lesions containing fibrous caps observed   (MGI Ref ID J:40136)
  • growth/size/body phenotype
  • decreased body weight
    • mice have decreased body weight until weaning when they will normalize their weight if fed a liquid diet   (MGI Ref ID J:40136)
  • hematopoietic system phenotype
  • abnormal osteoclast cell number   (MGI Ref ID J:33189)
    • decreased osteoclast cell number
      • at birth the osteoclast population appears normal but quickly decreases to negligible numbers by the time the mouse is 3-4 days of age   (MGI Ref ID J:33189)
  • abnormal osteoclast differentiation
    • exogenous M-CSF enables normal osteoclast differentiation   (MGI Ref ID J:38039)
  • immune system phenotype
  • abnormal osteoclast cell number   (MGI Ref ID J:33189)
    • decreased osteoclast cell number
      • at birth the osteoclast population appears normal but quickly decreases to negligible numbers by the time the mouse is 3-4 days of age   (MGI Ref ID J:33189)
  • abnormal osteoclast differentiation
    • exogenous M-CSF enables normal osteoclast differentiation   (MGI Ref ID J:38039)
  • skeleton phenotype
  • abnormal bone marrow cavity morphology
    • the excessive accumulations of bone lack marrow cavities   (MGI Ref ID J:5634)
  • abnormal bone remodeling
    • compared with normal littermates, bone matrix formation is significantly elevated before 40 days of age and significantly reduced between 81 days and 10 months of age   (MGI Ref ID J:5634)
    • although bone remodeling is reduced, overall decline in rate of bone formation removes excess bone resulting in nearly normal bone   (MGI Ref ID J:5634)
  • abnormal osteoclast cell number   (MGI Ref ID J:33189)
    • decreased osteoclast cell number
      • at birth the osteoclast population appears normal but quickly decreases to negligible numbers by the time the mouse is 3-4 days of age   (MGI Ref ID J:33189)
  • abnormal osteoclast differentiation
    • exogenous M-CSF enables normal osteoclast differentiation   (MGI Ref ID J:38039)
  • domed cranium
    • mutants are recognized at 10 days of age by a characteristic domed head   (MGI Ref ID J:5634)
  • craniofacial phenotype
  • absent teeth
    • noticeably absent at 10 days of age   (MGI Ref ID J:5634)
    • at weaning mice need to be provided with soft food in order to thrive   (MGI Ref ID J:5634)
  • domed cranium
    • mutants are recognized at 10 days of age by a characteristic domed head   (MGI Ref ID J:5634)
  • endocrine/exocrine gland phenotype
  • abnormal lactation
    • milk proteins are expressed but parturition does not initiate lactation   (MGI Ref ID J:20519)
  • abnormal mammary gland development   (MGI Ref ID J:20519)
    • abnormal branching of the mammary ductal tree
      • precocious development of the lobulo-alveolar system   (MGI Ref ID J:20519)
    • abnormal mammary gland growth during lactation
      • incomplete mammary gland ductal growth occurs during pregnancy   (MGI Ref ID J:20519)
  • abnormal mammary gland lobule morphology   (MGI Ref ID J:20519)
  • abnormal ovary morphology
    • very few macrophages present in ovaries at all stages of cycle and follicular development   (MGI Ref ID J:38039)
    • decreased corpora lutea number   (MGI Ref ID J:38039)
  • abnormal testis physiology
    • testosterone level in the tesis is lower than normal   (MGI Ref ID J:34371)
  • abnormal thyroid parafollicular C-cell morphology
    • this cell population is increased in this mutation   (MGI Ref ID J:5634)
  • reproductive system phenotype
  • abnormal ovary morphology
    • very few macrophages present in ovaries at all stages of cycle and follicular development   (MGI Ref ID J:38039)
    • decreased corpora lutea number   (MGI Ref ID J:38039)
  • abnormal ovulation
    • significantly lower ovulation rate and frequency   (MGI Ref ID J:38039)
    • decreased ovulation rate
      • 20% of ovaries fail to undergo ovulation   (MGI Ref ID J:38039)
      • the ovulation rate is low for mice that do ovulate   (MGI Ref ID J:38039)
  • abnormal proestrus
    • mice do not display the characteristic surge in circulating estradiol-17 beta expected during proestrus   (MGI Ref ID J:38039)
  • abnormal sperm number
    • a lower then normal number of viable sperm are detected   (MGI Ref ID J:34371)
    • normal numbers of viable sperm are restored after testosterone or CSF-1 treatment throughout the postnatal period   (MGI Ref ID J:34371)
  • abnormal testis physiology
    • testosterone level in the tesis is lower than normal   (MGI Ref ID J:34371)
  • decreased fertilization frequency
    • only 50% of the mated superovulated mutant females produced fertilized ooctyes compared with 83.3% of the mated superovulated heterozygous females   (MGI Ref ID J:38039)
  • decreased litter size   (MGI Ref ID J:38039)
  • impaired embryo implantation
    • a lower than normal number of implantations are seen   (MGI Ref ID J:38039)
  • prolonged estrous cycle
    • females reach estrus every 14 days compared with a normal approximately 5 day cycle   (MGI Ref ID J:38039)
    • subcutaneous adninistration of CSF-1 from birth restores a normal estrous cycle   (MGI Ref ID J:38039)
  • reduced female fertility   (MGI Ref ID J:38039)
  • integument phenotype
  • abnormal lactation
    • milk proteins are expressed but parturition does not initiate lactation   (MGI Ref ID J:20519)
  • abnormal mammary gland development   (MGI Ref ID J:20519)
    • abnormal branching of the mammary ductal tree
      • precocious development of the lobulo-alveolar system   (MGI Ref ID J:20519)
    • abnormal mammary gland growth during lactation
      • incomplete mammary gland ductal growth occurs during pregnancy   (MGI Ref ID J:20519)
  • abnormal mammary gland lobule morphology   (MGI Ref ID J:20519)
  • cellular phenotype
  • abnormal osteoclast differentiation
    • exogenous M-CSF enables normal osteoclast differentiation   (MGI Ref ID J:38039)

Csf1op/Csf1op

        B6;C3Fe a/a-Csf1op/J
  • immune system phenotype
  • abnormal microglial cell morphology
    • decrease in numbers of microglia in the white matter of the brain and spinal cord compared to wild-type mice   (MGI Ref ID J:170081)
  • decreased macrophage cell number
    • in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
    • numbers are significantly decreased in atral follicles   (MGI Ref ID J:30863)
    • numbers were enhanced by treatment with macrophage colony-stimulating factor   (MGI Ref ID J:30863)
  • impaired macrophage chemotaxis
    • to the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • homeostasis/metabolism phenotype
  • decreased physiological sensitivity to xenobiotic
    • mice are protected from bleomycin-induced lung fibrosis with fewer recruited alveolar macrophages in the bronchoalveolar lavage compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • hematopoietic system phenotype
  • abnormal microglial cell morphology
    • decrease in numbers of microglia in the white matter of the brain and spinal cord compared to wild-type mice   (MGI Ref ID J:170081)
  • decreased macrophage cell number
    • in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
    • numbers are significantly decreased in atral follicles   (MGI Ref ID J:30863)
    • numbers were enhanced by treatment with macrophage colony-stimulating factor   (MGI Ref ID J:30863)
  • impaired macrophage chemotaxis
    • to the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)
  • nervous system phenotype
  • abnormal microglial cell morphology
    • decrease in numbers of microglia in the white matter of the brain and spinal cord compared to wild-type mice   (MGI Ref ID J:170081)
  • abnormal neurite morphology
    • neurons explanted from embryonic day 17 cortex and cultured for 1 to 2 days have fewer processes and at 4 and 8 days of culture have decreased complexity of neurites compared with controls   (MGI Ref ID J:35818)
  • hearing/vestibular/ear phenotype
  • abnormal auditory brainstem response waveform shape
    • latencies are prolonged and amplitudes reduced with an absolute delay in the wave I latency, prolongation of the wave I-V interval, and loss of amlitude and integrity of the later components; subcutaneous administration of CSF1 daily for 10 weeks beginning at 2 days of age ameliorates this phenotype toward normal values   (MGI Ref ID J:35818)
  • vision/eye phenotype
  • abnormal visual evoked potential
    • surface visual evoked potentials are dramatically reduced or absent   (MGI Ref ID J:35818)
    • intracortical visual evoked potential readings show total intracortical current to be significantly reduced, both in the initial excitation and subsequent inhibition, with deficits found in both transmembrane current flow and multiple unit activity, although the onset latencies of current flow are normal; subcutaneous administration of CSF1 daily for 10 weeks beginning at 2 days of age ameliorates this phenotype toward normal values   (MGI Ref ID J:35818)
    • supragranular laminae and thalamorecipient layers both show abnormal processing   (MGI Ref ID J:35818)
    • administration of the GABA A antagonist bicuculline results not only in changes in neural firing in the supragranular laminae, as is the case in wild-type controls, but also results in diffusely elevated unit firing in several laminae in homozygotes indicating abnormal intracortical circuitry   (MGI Ref ID J:35818)
  • endocrine/exocrine gland phenotype
  • abnormal ovarian follicle number
    • there are fewer atral and mature follicles in the proestrus ovary compared with controls   (MGI Ref ID J:30863)
    • decreased mature ovarian follicle number   (MGI Ref ID J:30863)
    • decreased secondary ovarian follicle number
      • fewer follicles develop compared with normal   (MGI Ref ID J:30863)
  • abnormal ovarian folliculogenesis   (MGI Ref ID J:30863)
  • impaired granulosa cell differentiation
    • the numbers of cells in the atral follicles are significantly reduced but differentiation increases after treatment with macrophage colony-stimulating factor   (MGI Ref ID J:30863)
  • reproductive system phenotype
  • abnormal ovarian follicle number
    • there are fewer atral and mature follicles in the proestrus ovary compared with controls   (MGI Ref ID J:30863)
    • decreased mature ovarian follicle number   (MGI Ref ID J:30863)
    • decreased secondary ovarian follicle number
      • fewer follicles develop compared with normal   (MGI Ref ID J:30863)
  • abnormal ovarian folliculogenesis   (MGI Ref ID J:30863)
  • abnormal ovulation
    • total number of oocytes ovulated is less than expected   (MGI Ref ID J:30863)
    • the number of eggs ovulated at each cycle varies significantly   (MGI Ref ID J:30863)
  • impaired granulosa cell differentiation
    • the numbers of cells in the atral follicles are significantly reduced but differentiation increases after treatment with macrophage colony-stimulating factor   (MGI Ref ID J:30863)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mutants do not exhibit any neurological signs   (MGI Ref ID J:170081)
  • growth/size/body phenotype
  • abnormal postnatal growth
    • growth of mutants is slower than wild-type mice   (MGI Ref ID J:170081)
  • cellular phenotype
  • impaired granulosa cell differentiation
    • the numbers of cells in the atral follicles are significantly reduced but differentiation increases after treatment with macrophage colony-stimulating factor   (MGI Ref ID J:30863)
  • impaired macrophage chemotaxis
    • to the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147697)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Csf1op/Csf1op

        C57BL/6J-Csf1op
  • mortality/aging
  • premature death
    • 40% of mice that survive weaning die by 12 months   (MGI Ref ID J:5634)
    • hydrocephalus is observed in mice that die at an early age   (MGI Ref ID J:5634)
  • skeleton phenotype
  • abnormal osteoblast physiology
    • increased bone matrix formation to postnatal day 40   (MGI Ref ID J:5634)
    • decreased bone matrix formation after day 81   (MGI Ref ID J:5634)
  • abnormal skeleton morphology
    • overall skeleton is smaller than in wild-type   (MGI Ref ID J:110981)
    • abnormal bone structure
      • large lipoid masses in vascular and extravascular areas of bone   (MGI Ref ID J:5634)
      • abnormal bone marrow cavity morphology
        • delayed development of bone marrow cavity   (MGI Ref ID J:5634)
        • abnormally high numbers of megakaryocytes   (MGI Ref ID J:5634)
      • abnormal osteoclast morphology
        • osteoclasts small and few in number   (MGI Ref ID J:5634)
        • abnormal distribution of acid phosphatase activity   (MGI Ref ID J:5634)
        • decreased osteoclast cell number   (MGI Ref ID J:5634)
      • abnormal trabecular bone morphology
        • long bones filled with primary spongiosa   (MGI Ref ID J:5634)
      • osteopetrosis   (MGI Ref ID J:5634)
      • osteoporosis
        • mice exhibit osteoporosis   (MGI Ref ID J:110981)
    • domed cranium
      • observed by 10 days   (MGI Ref ID J:5634)
  • immune system phenotype
  • abnormal osteoclast morphology
    • osteoclasts small and few in number   (MGI Ref ID J:5634)
    • abnormal distribution of acid phosphatase activity   (MGI Ref ID J:5634)
    • decreased osteoclast cell number   (MGI Ref ID J:5634)
  • abnormal spleen red pulp morphology
    • sinusoids less developed   (MGI Ref ID J:5634)
  • decreased macrophage cell number
    • cells expressing F4/80+ (a marker for macrophages) are almost entirely absent   (MGI Ref ID J:110981)
    • decreased osteoclast cell number   (MGI Ref ID J:5634)
  • hematopoietic system phenotype
  • abnormal osteoclast morphology
    • osteoclasts small and few in number   (MGI Ref ID J:5634)
    • abnormal distribution of acid phosphatase activity   (MGI Ref ID J:5634)
    • decreased osteoclast cell number   (MGI Ref ID J:5634)
  • abnormal spleen red pulp morphology
    • sinusoids less developed   (MGI Ref ID J:5634)
  • decreased macrophage cell number
    • cells expressing F4/80+ (a marker for macrophages) are almost entirely absent   (MGI Ref ID J:110981)
    • decreased osteoclast cell number   (MGI Ref ID J:5634)
  • reproductive system phenotype
  • reduced fertility   (MGI Ref ID J:5634)
  • craniofacial phenotype
  • abnormal snout morphology
    • snouts are rounded   (MGI Ref ID J:110981)
  • absent incisors
    • absence of incisors is observed by 10 days   (MGI Ref ID J:5634)
  • absent teeth
    • homozygous mice are toothless   (MGI Ref ID J:110981)
  • domed cranium
    • observed by 10 days   (MGI Ref ID J:5634)
  • limbs/digits/tail phenotype
  • abnormal autopod morphology
    • all hind foot digits curve progressively laterally or medially   (MGI Ref ID J:5634)
    • change in shape of hind feet during growth, first digit of hindfoot often becomes parallel to the second digit   (MGI Ref ID J:5634)
  • short limbs   (MGI Ref ID J:5634)
  • short tail
    • frequent development of s-type curves   (MGI Ref ID J:5634)
  • growth/size/body phenotype
  • slow postnatal weight gain
    • from day 10 weight gain does not match control   (MGI Ref ID J:5634)
  • endocrine/exocrine gland phenotype
  • abnormal thyroid parafollicular C-cell morphology
    • parafollicular cell density in thyroid is significantly increased during first three months   (MGI Ref ID J:5634)
  • homeostasis/metabolism phenotype
  • decreased circulating phosphate level
    • serum phosphate levels average 30% below control   (MGI Ref ID J:5634)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Internal/Organ Research
Skeleton
      Bone

Neurobiology Research
Alzheimer's Disease
Parkinson's Disease

Csf1op related

Cancer Research
Growth Factors/Receptors/Cytokines

Developmental Biology Research
Skeletal Defects
      osteopetrosis

Endocrine Deficiency Research
Bone/Bone Marrow Defects

Immunology, Inflammation and Autoimmunity Research
Growth Factors/Receptors/Cytokines
Immunodeficiency
Immunodeficiency Associated with Other Defects

Research Tools
Immunology, Inflammation and Autoimmunity Research
      Macrophage Deficiency

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Csf1op
Allele Name osteopetrosis
Allele Type Spontaneous
Common Name(s) Csf-1op; Csf1- op; Csfmop; M-; csfmop; op;
Strain of OriginB6;DW-Pou1f1
Gene Symbol and Name Csf1, colony stimulating factor 1 (macrophage)
Chromosome 3
Gene Common Name(s) C87615; CSF-1; Csfm; M-CSF; MCSF; colony stimulating factor, macrophage; colony-stimulating factor-1; expressed sequence C87615; op; osteopetrosis;
General Note Phenotypic Similarity to Human Syndrome: Osteopetrosis, autosomal recessive in homozygous mice (J:26978)
Occlusion of the marrow cavities in young Csf1op/Csf1op mice leads to reduced hemopoiesis in the marrow, accompanied by splenomegaly and prolonged splenic hemopoiesis. The bone marrow is, however, seeded with the requisite hemopoietic precursor cells; and the reduced hemopoiesis in marrow is not due to direct effects of M-CSF (J:19549).

Bone marrow macrophages arrest in G1 phase in M-CSF deficient mice; the factor regulates cyclins involved in commitment of cells to S phase (J:14776). Bacterial translocation and lipopolysaccharide-induced morbidity and mortality are no different in Csf1op/Csf1op micethan in normal littermates (J:20379). Low levels of cytokines involved in immune reactions, found in 6 week old Csf1op homozygotes, recover to normal in these mice at older ages, as the bone marrow macrophage population is restored to normal (J:18531). Macrophage deficiencies in Csf1op/Csf1op mutants do not prevent them mounting normal T cell responses to infection (J:24207).

Intramuscular transplantation of myoblasts capable of producing M-CSF into Csf1ophomozygotes introduces the factor into the circulation of the mutant mice along with macrophages, but only transiently. The induced M-CSF may have been bound by macrophages accumulating at the site of the transplant. Macrophages accumulate at the site of muscle damage due to transplantation or to control muscle insult, and the damage can be repaired in the osteopetrotic mice (J:38812).

Molecular Note A single nucleotide (T) insertion 262 bp downstream from the initiation codon resulted in a frameshift and the creation of a stop codon 21 bp downstream of the insertion. [MGI Ref ID J:10519]
 
Allele Symbol a
Allele Name nonagouti
Allele Type Spontaneous
Strain of Originold mutant of the mouse fancy
Gene Symbol and Name a, nonagouti
Chromosome 2
Gene Common Name(s) AGSW; AGTI; AGTIL; ASP; As; SHEP9; agouti; agouti signal protein; agouti suppressor;
Molecular Note Characterization of this allele shows an insertion of DNA comprised of a 5.5kb virus-like element, VL30, into the first intron of the agouti gene. The VL30 element itself contains an additional 5.5 kb sequence, flanked by 526 bp of direct repeats. The host integration site is the same as for at-2Gso and Aw-38J and includes a duplication of four nucleotides of host DNA and a deletion of 2 bp from the end of each repeat. Northern analysis of mRNA from skin of homozygotes shows a smaller agouti message and levels 8 fold lower than found in wild-type. [MGI Ref ID J:16984] [MGI Ref ID J:24934]

Genotyping

Genotyping Information

Genotyping Protocols

Csf1op/J, Fluorescent PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Bruhns P; Samuelsson A; Pollard JW; Ravetch JV. 2003. Colony-stimulating factor-1-dependent macrophages are responsible for IVIG protection in antibody-induced autoimmune disease. Immunity 18(4):573-81. [PubMed: 12705859]  [MGI Ref ID J:83013]

Ida-Yonemochi H; Noda T; Shimokawa H; Saku T. 2002. Disturbed tooth eruption in osteopetrotic (op/op) mice: histopathogenesis of tooth malformation and odontomas. J Oral Pathol Med 31(6):361-73. [PubMed: 12201247]  [MGI Ref ID J:78487]

Kaku M; Tsutsui K; Motokawa M; Kawata T; Fujita T; Kohno S; Tohma Y; Ohtani J; Tenjoh K; Tanne K. 2003. Amyloid beta protein deposition and neuron loss in osteopetrotic (op/op) mice. Brain Res Brain Res Protoc 12(2):104-8. [PubMed: 14613812]  [MGI Ref ID J:87261]

Lenda DM; Kikawada E; Stanley ER; Kelley VR. 2003. Reduced macrophage recruitment, proliferation, and activation in colony-stimulating factor-1-deficient mice results in decreased tubular apoptosis during renal inflammation. J Immunol 170(6):3254-62. [PubMed: 12626584]  [MGI Ref ID J:82301]

Lenda DM; Stanley ER; Kelley VR. 2004. Negative role of colony-stimulating factor-1 in macrophage, T cell, and B cell mediated autoimmune disease in MRL-Fas(lpr) mice. J Immunol 173(7):4744-54. [PubMed: 15383612]  [MGI Ref ID J:93714]

Naito M; Hayashi S; Yoshida H; Nishikawa S; Shultz LD; Takahashi K. 1991. Abnormal differentiation of tissue macrophage populations in 'osteopetrosis' (op) mice defective in the production of macrophage colony-stimulating factor. Am J Pathol 139(3):657-67. [PubMed: 1887865]  [MGI Ref ID J:26978]

Sasaki A; Yokoo H; Naito M; Kaizu C; Shultz LD; Nakazato Y. 2000. Effects of macrophage-colony-stimulating factor deficiency on the maturation of microglia and brain macrophages and on their expression of scavenger receptor. Neuropathology 20(2):134-42. [PubMed: 10935450]  [MGI Ref ID J:82594]

Tagaya H; Kunisada T; Yamazaki H; Yamane T; Tokuhisa T; Wagner EF; Sudo T; Shultz LD; Hayashi SI. 2000. Intramedullary and extramedullary B lymphopoiesis in osteopetrotic mice. Blood 95(11):3363-70. [PubMed: 10828017]  [MGI Ref ID J:82593]

Yoshida H; Hayashi S; Kunisada T; Ogawa M; Nishikawa S; Okamura H; Sudo T; Shultz LD; Nishikawa S. 1990. The murine mutation osteopetrosis is in the coding region of the macrophage colony stimulating factor gene. Nature 345(6274):442-4. [PubMed: 2188141]  [MGI Ref ID J:10519]

Csf1op related

Abboud SL; Woodruff K; Liu C; Shen V; Ghosh-Choudhury N. 2002. Rescue of the osteopetrotic defect in op/op mice by osteoblast-specific targeting of soluble colony-stimulating factor-1. Endocrinology 143(5):1942-9. [PubMed: 11956177]  [MGI Ref ID J:76327]

Alnaeeli M; Penninger JM; Teng YT. 2006. Immune interactions with CD4+ T cells promote the development of functional osteoclasts from murine CD11c+ dendritic cells. J Immunol 177(5):3314-26. [PubMed: 16920972]  [MGI Ref ID J:139526]

Araki M; Fukumatsu Y; Katabuchi H; Shultz LD; Takahashi K; Okamura H. 1996. Follicular development and ovulation in macrophage colony-stimulating factor-deficient mice homozygous for the osteopetrosis (op) mutation. Biol Reprod 54(2):478-84. [PubMed: 8788202]  [MGI Ref ID J:30863]

Banaei-Bouchareb L; Gouon-Evans V; Samara-Boustani D; Castellotti MC; Czernichow P; Pollard JW; Polak M. 2004. Insulin cell mass is altered in Csf1op/Csf1op macrophage-deficient mice. J Leukoc Biol 76(2):359-67. [PubMed: 15178709]  [MGI Ref ID J:91463]

Baran CP; Opalek JM; McMaken S; Newland CA; O'Brien JM Jr; Hunter MG; Bringardner BD; Monick MM; Brigstock DR; Stromberg PC; Hunninghake GW; Marsh CB. 2007. Important roles for macrophage colony-stimulating factor, CC chemokine ligand 2, and mononuclear phagocytes in the pathogenesis of pulmonary fibrosis. Am J Respir Crit Care Med 176(1):78-89. [PubMed: 17431224]  [MGI Ref ID J:147697]

Batchelor PE; Porritt MJ; Nilsson SK; Bertoncello I; Donnan GA; Howells DW. 2002. Periwound dopaminergic sprouting is dependent on numbers of wound macrophages. Eur J Neurosci 15(5):826-32. [PubMed: 11906524]  [MGI Ref ID J:107999]

Begg SK; Radley JM; Pollard JW; Chisholm OT; Stanley ER; Bertoncello I. 1993. Delayed hematopoietic development in osteopetrotic (op/op) mice. J Exp Med 177(1):237-42. [PubMed: 8418205]  [MGI Ref ID J:3480]

Berezovskaya O; Maysinger D; Fedoroff S. 1995. The hematopoietic cytokine, colony-stimulating factor 1, is also a growth factor in the CNS: congenital absence of CSF-1 in mice results in abnormal microglial response and increased neuron vulnerability to injury. Int J Dev Neurosci 13(3-4):285-99. [PubMed: 7572282]  [MGI Ref ID J:30212]

Bergmann CE; Hoefer IE; Meder B; Roth H; van Royen N; Breit SM; Jost MM; Aharinejad S; Hartmann S; Buschmann IR. 2006. Arteriogenesis depends on circulating monocytes and macrophage accumulation and is severely depressed in op/op mice. J Leukoc Biol 80(1):59-65. [PubMed: 16684892]  [MGI Ref ID J:110465]

Blevins G; Fedoroff S. 1995. Microglia in colony-stimulating factor 1-deficient op/op mice. J Neurosci Res 40(4):535-44. [PubMed: 7616613]  [MGI Ref ID J:23600]

Brown NJ; Hutcheson J; Bickel E; Scatizzi JC; Albee LD; Haines GK 3rd; Eslick J; Bradley K; Taricone E; Perlman H. 2004. Fas death receptor signaling represses monocyte numbers and macrophage activation in vivo. J Immunol 173(12):7584-93. [PubMed: 15585886]  [MGI Ref ID J:94851]

Bruhns P; Samuelsson A; Pollard JW; Ravetch JV. 2003. Colony-stimulating factor-1-dependent macrophages are responsible for IVIG protection in antibody-induced autoimmune disease. Immunity 18(4):573-81. [PubMed: 12705859]  [MGI Ref ID J:83013]

Buchholz BM; Chanthaphavong RS; Bauer AJ. 2009. Nonhemopoietic cell TLR4 signaling is critical in causing early lipopolysaccharide-induced ileus. J Immunol 183(10):6744-53. [PubMed: 19846874]  [MGI Ref ID J:157181]

Carenini S; Maurer M; Werner A; Blazyca H; Toyka KV; Schmid CD; Raivich G; Martini R. 2001. The role of macrophages in demyelinating peripheral nervous system of mice heterozygously deficient in p0. J Cell Biol 152(2):301-8. [PubMed: 11266447]  [MGI Ref ID J:67581]

Cecchini MG; Dominguez MG; Mocci S; Wetterwald A; Felix R; Fleisch H; Chisholm O; Hofstetter W; Pollard JW; Stanley ER. 1994. Role of colony stimulating factor-1 in the establishment and regulation of tissue macrophages during postnatal development of the mouse. Development 120(6):1357-72. [PubMed: 8050349]  [MGI Ref ID J:18915]

Chang MD; Stanley ER; Khalili H; Chisholm O; Pollard JW. 1995. Osteopetrotic (op/op) mice deficient in macrophages have the ability to mount a normal T-cell-dependent immune response. Cell Immunol 162(1):146-52. [PubMed: 7704903]  [MGI Ref ID J:24207]

Chang Y; Albright S; Lee F. 1994. Cytokines in the central nervous system: expression of macrophage colony stimulating factor and its receptor during development. J Neuroimmunol 52(1):9-17. [PubMed: 8207122]  [MGI Ref ID J:19249]

Choi JH; Cheong C; Dandamudi DB; Park CG; Rodriguez A; Mehandru S; Velinzon K; Jung IH; Yoo JY; Oh GT; Steinman RM. 2011. Flt3 Signaling-Dependent Dendritic Cells Protect against Atherosclerosis. Immunity 35(5):819-31. [PubMed: 22078798]  [MGI Ref ID J:178831]

Clohisy DR; Ramnaraine ML. 1997. Osteoclast formation during tumor osteolysis does not require proliferating osteoclast precursor cells. J Orthop Res 15(2):301-6. [PubMed: 9167635]  [MGI Ref ID J:41527]

Clynes R; Ravetch JV. 1995. Cytotoxic antibodies trigger inflammation through Fc receptors. Immunity 3(1):21-6. [PubMed: 7621075]  [MGI Ref ID J:78887]

Cohen PE; Chisholm O; Arceci RJ; Stanley ER; Pollard JW. 1996. Absence of colony-stimulating factor-1 in osteopetrotic (csfmop/csfmop) mice results in male fertility defects. Biol Reprod 55(2):310-7. [PubMed: 8828834]  [MGI Ref ID J:34371]

Cohen PE; Hardy MP; Pollard JW. 1997. Colony-stimulating factor-1 plays a major role in the development of reproductive function in male mice. Mol Endocrinol 11(11):1636-50. [PubMed: 9328346]  [MGI Ref ID J:43181]

Cohen PE; Zhu L; Pollard JW. 1997. Absence of colony stimulating factor-1 in osteopetrotic (csfmop/csfmop) mice disrupts estrous cycles and ovulation. Biol Reprod 56(1):110-8. [PubMed: 9002639]  [MGI Ref ID J:38039]

D'Errico JA; MacNeil RL; Strayhorn CL; Piotrowski BT; Somerman MJ. 1995. Models for the study of cementogenesis. Connect Tissue Res 33(1-3):9-17. [PubMed: 7554968]  [MGI Ref ID J:30202]

Dai XM; Ryan GR; Hapel AJ; Dominguez MG; Russell RG; Kapp S; Sylvestre V; Stanley ER. 2002. Targeted disruption of the mouse colony-stimulating factor 1 receptor gene results in osteopetrosis, mononuclear phagocyte deficiency, increased primitive progenitor cell frequencies, and reproductive defects. Blood 99(1):111-20. [PubMed: 11756160]  [MGI Ref ID J:73663]

Dai XM; Zong XH; Sylvestre V; Stanley ER. 2004. Incomplete restoration of colony-stimulating factor 1 (CSF-1) function in CSF-1-deficient Csf1op/Csf1op mice by transgenic expression of cell surface CSF-1. Blood 103(3):1114-23. [PubMed: 14525772]  [MGI Ref ID J:87641]

De Ciuceis C; Amiri F; Brassard P; Endemann DH; Touyz RM; Schiffrin EL. 2005. Reduced vascular remodeling, endothelial dysfunction, and oxidative stress in resistance arteries of angiotensin II-infused macrophage colony-stimulating factor-deficient mice: evidence for a role in inflammation in angiotensin-induced vascular injury. Arterioscler Thromb Vasc Biol 25(10):2106-13. [PubMed: 16100037]  [MGI Ref ID J:114425]

Deckers MM; Van Beek ER; Van Der Pluijm G; Wetterwald A; Van Der Wee-Pals L; Cecchini MG; Papapoulos SE; Lowik CW. 2002. Dissociation of angiogenesis and osteoclastogenesis during endochondral bone formation in neonatal mice. J Bone Miner Res 17(6):998-1007. [PubMed: 12054176]  [MGI Ref ID J:112373]

Dhawan J; Rando TA; Elson SE; Lee F; Stanley ER; Blau HM. 1996. Myoblast-mediated expression of colony stimulating factor-1 (CSF-1) in the cytokine-deficient op/op mouse. Somat Cell Mol Genet 22(5):363-81. [PubMed: 9039846]  [MGI Ref ID J:38812]

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Feuerer M; Herrero L; Cipolletta D; Naaz A; Wong J; Nayer A; Lee J; Goldfine AB; Benoist C; Shoelson S; Mathis D. 2009. Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters. Nat Med 15(8):930-9. [PubMed: 19633656]  [MGI Ref ID J:152186]

Fujimoto W; Shiuchi T; Miki T; Minokoshi Y; Takahashi Y; Takeuchi A; Kimura K; Saito M; Iwanaga T; Seino S. 2007. Dmbx1 is essential in agouti-related protein action. Proc Natl Acad Sci U S A 104(39):15514-9. [PubMed: 17873059]  [MGI Ref ID J:125193]

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Galbraith DB; Patrignani AM. 1976. Sulfhydryl compounds in melanocytes of yellow (Ay/a), nonagouti (a/a), and agouti (A/A) mice. Genetics 84(3):587-91. [PubMed: 1001879]  [MGI Ref ID J:5737]

Galbraith DB; Wolff GL; Brewer NL. 1980. Hair pigment patterns in different integumental environments of the mouse. Influence of the agouti suppressor (A<s>) mutation on expression of agouti locus alleles. J Hered 71:229-234.  [MGI Ref ID J:12033]

Galbraith DB; Wolff GL; Brewer NL. 1979. Tissue microenvironment and the genetic control of hair pigment patterns in mice Dev Genet 1(2):167-179.  [MGI Ref ID J:156092]

Geschwind II; Huseby RA; Nishioka R. 1972. The effect of melanocyte-stimulating hormone on coat color in the mouse. Recent Prog Horm Res 28:91-130. [PubMed: 4631622]  [MGI Ref ID J:5324]

Granholm DE; Reese RN; Granholm NH. 1996. Agouti alleles alter cysteine and glutathione concentrations in hair follicles and serum of mice (A y/a, A wJ/A wJ, and a/a). J Invest Dermatol 106(3):559-63. [PubMed: 8648194]  [MGI Ref ID J:32132]

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Hearing VJ; Phillips P; Lutzner MA. 1973. The fine structure of melanogenesis in coat color mutants of the mouse. J Ultrastruct Res 43(1):88-106. [PubMed: 4634048]  [MGI Ref ID J:5346]

Hustad CM; Perry WL; Siracusa LD; Rasberry C; Cobb L; Cattanach BM; Kovatch R; Copeland NG; Jenkins NA. 1995. Molecular genetic characterization of six recessive viable alleles of the mouse agouti locus. Genetics 140(1):255-65. [PubMed: 7635290]  [MGI Ref ID J:24934]

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Kaelin CB; Xu X; Hong LZ; David VA; McGowan KA; Schmidt-Kuntzel A; Roelke ME; Pino J; Pontius J; Cooper GM; Manuel H; Swanson WF; Marker L; Harper CK; van Dyk A; Yue B; Mullikin JC; Warren WC; Eizirik E; Kos L; O'Brien SJ; Barsh GS; Menotti-Raymond M. 2012. Specifying and sustaining pigmentation patterns in domestic and wild cats. Science 337(6101):1536-41. [PubMed: 22997338]  [MGI Ref ID J:188277]

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Novak EK; Gautam R; Reddington M; Collinson LM; Copeland NG; Jenkins NA; McGarry MP; Swank RT. 2002. The regulation of platelet-dense granules by Rab27a in the ashen mouse, a model of Hermansky-Pudlak and Griscelli syndromes, is granule-specific and dependent on genetic background. Blood 100(1):128-35. [PubMed: 12070017]  [MGI Ref ID J:77395]

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Nuotio-Antar AM; Hachey DL; Hasty AH. 2007. Carbenoxolone treatment attenuates symptoms of metabolic syndrome and atherogenesis in obese, hyperlipidemic mice. Am J Physiol Endocrinol Metab 293(6):E1517-28. [PubMed: 17878220]  [MGI Ref ID J:145108]

Papacleovoulou G; Abu-Hayyeh S; Nikolopoulou E; Briz O; Owen BM; Nikolova V; Ovadia C; Huang X; Vaarasmaki M; Baumann M; Jansen E; Albrecht C; Jarvelin MR; Marin JJ; Knisely AS; Williamson C. 2013. Maternal cholestasis during pregnancy programs metabolic disease in offspring. J Clin Invest 123(7):3172-81. [PubMed: 23934127]  [MGI Ref ID J:201610]

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Rakyan VK; Chong S; Champ ME; Cuthbert PC; Morgan HD; Luu KV; Whitelaw E. 2003. Transgenerational inheritance of epigenetic states at the murine Axin(Fu) allele occurs after maternal and paternal transmission. Proc Natl Acad Sci U S A 100(5):2538-43. [PubMed: 12601169]  [MGI Ref ID J:82396]

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Rosenfeld CS; Sieli PT; Warzak DA; Ellersieck MR; Pennington KA; Roberts RM. 2013. Maternal exposure to bisphenol A and genistein has minimal effect on A(vy)/a offspring coat color but favors birth of agouti over nonagouti mice. Proc Natl Acad Sci U S A 110(2):537-42. [PubMed: 23267115]  [MGI Ref ID J:193279]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           FGB27

Colony Maintenance

Breeding & HusbandryHomozygous pups (produced by a het x het mating) are identifiable by their phenotype at 10 days of age by absence of incisors and by a domed skull. Unfortunately, ~50% of homozygotes die around weaning age. If they are to survive the weaning process, they must be provided with crushed food in the bottom of the cage. A soft rodent diet could also be used. Those that survive weaning may live up to 6 months.
Mating SystemHeterozygous x B6C3FeF1/J a/a Stock No. 001022
B6C3FeF1/J a/a Stock No. 001022 x Heterozygous
Diet Information LabDiet® 5K52/5K67

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Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $195.00Female or MaleHeterozygous for Csf1op  
Price per Pair (US dollars $)Pair Genotype
$320.00B6C3FeF1/J a/a (001022) x Heterozygous for Csf1op  
$320.00Heterozygous for Csf1op x B6C3FeF1/J a/a (001022)  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Supply Notes

  • Homozygous animals are not available due to the severity of the phenotype and the mortality rate (50% of animals do not survive to weaning age).
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $253.50Female or MaleHeterozygous for Csf1op  
Price per Pair (US dollars $)Pair Genotype
$416.00B6C3FeF1/J a/a (001022) x Heterozygous for Csf1op  
$416.00Heterozygous for Csf1op x B6C3FeF1/J a/a (001022)  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Supply Notes

  • Homozygous animals are not available due to the severity of the phenotype and the mortality rate (50% of animals do not survive to weaning age).
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

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  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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