| Title | Phenotype | Contact | |
|---|---|---|---|
| B6.129-Flrt2<tm1Rob>/RobH | Mouse embryos deficient in Flrt2 display defects in heart morphogenesis, in particular, defects in the integrity of the epicardium and disturbances to the architecture of the underlying basement membrane accompanied by a pronounced reduction in thickness of the ventricular myocardium. A small proportion of homozygous mutants survive gestation (<3%). Heterozygous mice have no overt phenotype. | Contact | |
| B6.129-Flrt3<tm1Rob>/RobH | Mouse embryos deficient in Flrt3 display defects in headfold fusion, definitive endoderm migration and a failure of the lateral edges of the ventral body wall to fuse, leading to cardia bifida. A small proportion of homozygous mutants survive gestation and develop as viable fertile animals (<3%). Heterozygous mice have no overt phenotype. | Contact | |
| B6.129-Krt36<tm1Hpt>/H | Hyperkeratosis of scales (tail) and filiform papillae (tongue). The analyses are not yet complete but if present, the phenotype is very weak in heterozygotes. An obvious hyperkeratosis is however apparent in homozygous mutant animals. | Contact | |
| B6.129-Mrc2<tm1Cmi>/H | Homozygous Endo180DeltaEx2-6/Endo180DeltaEx2-6 mice are phenotypically normal (at the gross level), healthy and fertile. | Contact | |
| B6.129-Nrxn2<tm1Sud>/H | Mice homozygous for a knock-out allele show a 30-40% decrease in body weight and their inhibitory postsynaptic currents (IPSCs) are decreased in cortical slice cultures. Further phenotyping data to be published shortly. | Contact | |
| B6.129-Prdm1<tm1.1Liz>/RobH | No overt phenotype. Mice with targeted exon 1A deletion show that Prdm1 expression has been eliminated in LPS-stimulated B cells and plasma cell differentiation has been blocked. Embryonic development is not disrupted, and embryos with this deletion show modestly reduced Prdm1 expression levels. | Contact | |
| B6.129-Prdm1<tm1.1Liz>/RobH | No overt phenotype. Mice with targeted exon 1A deletion show that Prdm1 expression has been eliminated in LPS-stimulated B cells and plasma cell differentiation has been blocked. Embryonic development is not disrupted, and embryos with this deletion show modestly reduced Prdm1 expression levels. | Contact | |
| B6.129-Prdm1<tm2.1Liz>/RobH | No overt phenotype. Mice with targeted exon 1B deletion have slightly decreased expression in the yolk sac but show no other noticeable effects in embryo or adult tissues. | Contact | |
| B6.129-Prdm1<tm3.1Liz>/RobH | Homozygotes are lethal and die around E10.5 due to placental defects. Heterozygotes have no overt phenotype. | Contact | |
| B6.129-Prdm1<tm4.1Liz>/RobH | Homozygotes and heterozygotes show no overt phenotype. | Contact | |
| B6.129-Prdm4<tm2.1Liz>/RobH | Mice with targeted deletion of the zinc finger domain have no phenotype. Heterozygotes also have no overt phenotype. | Contact | |
| B6.129-S100A10<tm1Jnw>/H | None. | Contact | |
| B6.129-Scn10a<tm2(cre)Jnw>/H | No phenotype in heterozygotes. Some pain deficits in homozygotes. | Contact | |
| B6.129-Scn10a<tm2(cre)Jnw>/H | No phenotype in heterozygotes. Some pain deficits in homozygotes. | Contact | |
| B6.129-Tln2<tm2Crit>/CritH | The homozygous Tln2(cd) mice are viable and fertile, and exhibit no evidence of any phenotype. | Contact | |
| B6.129P2(C)-Igf2<tm4.1Wrk>/H | Loss of Igf2 imprinting. | Contact | |
| B6.129P2(Cg)-Dazl<tm1Hjc>/H | Mice homozygous for this mutation in this background lack germ cells at birth in both sexes. Heterozygous mice show close to normal fertility. | Contact | |
| B6.129P2(Cg)-Fgfr3<tm1.1Aomw>/Aomw | All homozygous males, some homozygous females and some heterozygous males develop an abnormal skull phenotype sometimes with malocclusion, and may be smaller in size. The phenotype is not fully penetrant. | Contact | |
| B6.129P2(Cg)-Il1rn<tm1Nick>/Nick | Strain resistant to arthritis, arteritis and psoriasis (seen in BALB/c) but highly susceptible to undefined 'malaise' under conventional conditions. | Contact | |
| B6.129P2(Cg)-Tlx1<tm1Thr>/H | Asplenia. | Contact |
