| First Author | Artzt K | Year | 1987 |
| Journal | Dev Genet | Volume | 8 |
| Issue | 1 | Pages | 1-9 |
| PubMed ID | 3502964 | Mgi Jnum | J:9377 |
| Mgi Id | MGI:57838 | Doi | 10.1002/dvg.1020080102 |
| Citation | Artzt K, et al. (1987) Ovarian teratocarcinomas in LT/Sv mice carrying t-mutations. Dev Genet 8(1):1-9 |
| abstractText | Ovarian teratomas that result from parthenogenetic activation of oocytes provide a double tool for developmental genetics. First, they provide a way of measuring recombination between a gene and its centromere. Second, in the absence of crossing over there is the potential of producing tumors that are homozygous for genes that would be lethal in the course of in utero embryonic development. We have applied both aspects to several t-haplotypes containing different early acting t-lethal genes. In a study of 26 tumors, genotyped by Southern blot analysis of the major histocompatibility complex (MHC), we measured the distance between the centromere and the start of the t-complex as 5.6 +/- 2.3 cM. We found a marked deficiency of t-homozygous genotypes among the tumors we studied, although T/T genotypes formed teratomas at levels comparable to controls. None of the lethal t-haplotypes we studied permit homozygous embryos to develop to the primitive streak stage, while T/T embryos do develop essentially normally through that stage. Thus, although the total number of tumors observed from t-bearing mice was small, the great difference in the incidence of t/t tumors versus the incidence of T/T tumors suggests strongly that the parthenogenetic embryos that convert to teratocarcinomas must first pass through some of the stages of normal early development, including the formation of three germ layers and the primitive streak. |
