JAX Mice Database - (cleft palate)

Search Criteria: Research Area is "Developmental Biology Research: Craniofacial and Palate Defects (cleft palate)"

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
006229	B6.Cg-Tg(DRE-lacZ)2Gswz/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Following adult or in utero exposure with xenobiotic ligands (including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs)), lacZ expression is induced in tissues targeted by the toxic compounds; for example, embryonic tissues expressing beta-galactosidase following TCDD treatment in utero include hard and soft palates, genital tubercle, certain facial regions, shoulder, and other tissues). These mice may be useful in studies of toxicology, teratogenic and xenobiotic processes, Per-Arnt-Sim transcription factors, cleft-palate, and as a reporter strain to indicate the temporal and spatial context of transcriptionally active aryl hydrocarbon receptors following agonist exposure in vivo.
005709	B6.129-Ski^tm1Cco/J	Repository-Cryopreserved
	This mutant was created on a mixed (129 x C57BL/6J) background. Greater than 80% of mice on this mixed background had severe neural tube closure defects (such as exencephaly) while less than 16% exhibited facial clefting. The penetrance of these phenotypes has segregated with further backcross to C57BL/6J. The congenic mutant described here was backcrossed 12-14 times to wildtype C57BL/6J. Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. Null mice are distinguishable from wildtype and heterozygous littermates at embryonic day 8.5 (E8.5) with delayed, but complete, cranial neural tube closure (incomplete at the normal E9.5). Ninety percent of null mice alive at E18.5 exhibit facial clefting. Other highly penetrant phenotypes include flattened snout, depressed nasal bridge, excessive orbital separation, elongated subventricular zones, vestigial polydactyly, and malformations of the olfactory bulb, iris, and ventral septum. Heterozy ..... For more information please see the full descriiption on the strain data sheet
002619	B6.129-Tgfb3^tm1Doe/J	Repository-Cryopreserved
	Mice homozygous for the Tgfb3^tm1Doe mutation are not viable. Mice exhibit cleft palate and possibly developmental defects in the lung.
006382	B6;129-Cask^tm1Sud/J	Repository-Cryopreserved
	Homozygous floxed mice are viable and fertile, but females do not thrive. The body size of mutants is significantly smaller than littermate controls and they exhibit a slightly increased mortality. Knock-in mice are hypomorphs and protein is expressed at less than 30% of normal levels. Crossing of the floxed mutants with mice expressing cre recombinase in the male germline excises the floxed exon and a neomycin resistance gene cassette to create a complete knockout of the gene. Knockout homozygotes die within a few hours of birth. They exhibit a partially penetrant cleft palate syndrome and increased apoptosis in the thalamus, but display no other major developmental changes or deficits in basic electrical properties of their neurons. When bred to a strain expressing Cre recombinase in the male germline (see Stock No. 003328 or 007252 for example), this mutant mouse str ..... For more information please see the full descriiption on the strain data sheet
000515	B6CBACa A^w-J/A-Sfn^Er/J	Repository-Cryopreserved

001747	STOCK Oca2^p-d/Oca2^p-cp/J	Repository-Cryopreserved
	Mice homozygous for Oca2^p-d (dark pink-eye) are born with lightly pigmented eyes, darker than those of Oca2^p/Oca2^p mice, which darken by weaning and a coat color "considerably darker than that of Oca2^p/Oca2^p mice, somewhat resembling that of brown [Tyrp1^b/Tyrp1^b] mice"; both sexes are fertile (Gardner et al. 1977, Lyon et al. 1992). A normal-sized Oca2^p transcript is present in eyes of Oca2^p-d/Oca2^p-d mice (Gardner et al. 1992), and Southern blot analysis revealed no gross alteration of the Oca2^p gene (Gardner et al. 1992, Lyon et al. 1992); thus, the molecular nature of the defect is unknown. Most Oca2^p-cp (p-cleft palate, formerly p^11H) homozygotes die soon after birth with cleft palate; the few that survive to adulthood exhibit significant dilution of coat co ..... For more information please see the full descriiption on the strain data sheet

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