Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation +pN1 Generation Definitions   Donating Investigator Dr. Joachim Herz,   Univ of Texas Southwest Med Ctr Dallas

Description
The FE65 knockout allele has a nuclear localized-lacZ replacing exon 2 of the Apbb1 gene. No protein expression is detected from the mutant locus, and the donating investigator reports that whether lacZ staining faithfully reflects FE65 expression has not been conclusively resolved. Homozygous (FE65-/-) mice are viable, fertile, and indistinguishable from wildtype littermates. Histological examination of adult brains shows no obvious neuroanatomical abnormalities. These FE65 mutant mice may be useful in studying brain development (neuronal positioning and establishment of axonal projections) and abnormal brain morphology (Cobblestone Lissencephaly, marginal zone heterotopias, and pial basement membrane integrity); as well as the function of FE65 family proteins in amyloid precursor protein (APP) processing, Alzheimer's disease, and neuronal protein trafficking.

For example, mice homozygous for both this FE65 knockout allele and the FE65L1 knockout allele (see Stock No. 012869) exhibit postnatal lethality (partial penetrance), are smaller than their wildtype or heterozygous littermates, and often display bilateral circling. While routine histological staining of the major organs in double knockout (FE65-/-;FE65L1-/-) mice reveals no overt anatomical abnormalities, FE65-/-;FE65L1-/- mice display cortical dysplasia with heterotopias resembling those of Cobblestone Lissencephaly. Specifically, FE65-/-;FE65L1-/- mice exhibit neuroanatomical abnormalities in the cortex and hippocampus that include marginal zone heterotopias (migration of heterotopic neurons beyond the marginal zone and located in the wrong part of the brain), midline crossing defects, and axonal pathfinding abnormalities. The phenotype of FE65-/-;FE65L1-/- mice shares remarkable similarities with that reported for mutant mice lacking FE65-binding partners, the three members of the APP gene family (APP, APLP1 and APLP2), and the Ena/Vasp protein family.

Development
These FE65 mutant mice were created in the laboratory of Dr. Joachim Herz (University of Texas Southwestern Medical Center, Dallas). A targeting vector was designed to replace 6.5 kb of the FE65 (Apbb1) locus (including the C-terminal 77 nucleotides of exon 2, intron 2 and the N-terminal 158 nucleotides of exon 3) with a β-galactosidase (lacZ) with nuclear localization signal and oppositely-oriented pol2neo cassette. This construct was electroporated into 129S6/SvEvTac-derived SM1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts and chimeric males were bred with C57BL/6J inbred females to establish the colony. Mutant mice were then bred together for several generations and made homozygous. Therefore, homozygous mice on a mixed C57BL/6J;129SvEvTac genetic background (not C57BL/6;129SvEvBradley as originally reported) were sent to The Jackson Laboratory Repository. Upon arrival, mice were bred to C57BL/6J (Stock No. 000664) for at least one generation to establish the colony.

Control Information

	Control
	Wild-type from the colony
	101043 B6129SF1/J	(approximate)
	101045 B6129SF2/J	(approximate)
Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Apbb1

005708

B6.129-Apbb1tm1Quhu/J

View Strains carrying other alleles of Apbb1     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Apbb1^tm1Her/Apbb1^tm1Her

        involves: 129S6/SvEvTac * C57BL/6

• normal phenotype
• no abnormal phenotype detected
  • homozygotes are viable and fertile with normal brain morphology   (MGI Ref ID J:105160)

View Research Applications

Research Applications

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

Cell Biology Research
Defects in Cell Adhesion Molecules
Signal Transduction

Developmental Biology Research
Defects in Cell Adhesion Molecules
Internal/Organ Defects
      brain
Neurodevelopmental Defects

Mouse/Human Gene Homologs
autosomal recessive lissencephaly

Neurobiology Research
Alzheimer's Disease
Ataxia (Movement) Defects
Cortical Defects
Neurodevelopmental Defects
Receptor Defects

Research Tools
Neurobiology Research

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Apbb1tm1Her
Allele Name		targeted mutation 1, Joachim Herz
Allele Type		Targeted (knock-out)
Common Name(s)		Apbb1tm1Sgnt; Fe65-; p97/60FE65-;
Mutation Made By		Dr. Joachim Herz,   Univ of Texas Southwest Med Ctr Dallas
Strain of Origin		129S6/SvEvTac
Gene Symbol and Name		Apbb1, amyloid beta (A4) precursor protein-binding, family B, member 1
Chromosome		7
Gene Common Name(s)		FE65; MGC:9072; RIR; Rir; retroviral integrase related;
Molecular Note		A targeting vector was designed to replace 6.5 kb of sequence with a pol2neo cassette and a lacZ into exon 2. Deleted sequence contained the C-terminal 77 nucleotides of exon 2, intron 2 and the N-terminal 158 nucleotides of exon 3. Protein was not detected by Western blot analysis. [MGI Ref ID J:105160]

Genotyping

Genotyping Information

Genotyping Protocols

Apbb1^tm1Her, Separated PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Apbb1^tm1Her related

Forni PE; Fornaro M; Guenette S; Wray S. 2011. A role for FE65 in controlling GnRH-1 neurogenesis. J Neurosci 31(2):480-91. [PubMed: 21228158]  [MGI Ref ID J:168231]

Guenette S; Chang Y; Hiesberger T; Richardson JA; Eckman CB; Eckman EA; Hammer RE; Herz J. 2006. Essential roles for the FE65 amyloid precursor protein-interacting proteins in brain development. EMBO J 25(2):420-31. [PubMed: 16407979]  [MGI Ref ID J:105160]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & Husbandry	When maintaining a live colony, homozygous mice may be bred together.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

Control Information

	Control
	Wild-type from the colony
	101043 B6129SF1/J	(approximate)
	101045 B6129SF2/J	(approximate)
Considerations for Choosing Controls
Control Pricing Information for Genetically Engineered Mutant Strains.

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The Jackson Laboratory's Genotype Promise

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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