Assuntos
Camundongos/genética , Leveduras/genética , Animais , Sequência de Bases , Mapeamento Cromossômico , Feminino , Genes Fúngicos , Ligação Genética , Heterozigoto , Humanos , Masculino , Camundongos Endogâmicos BALB C , Dados de Sequência Molecular , Oócitos/citologia , Gravidez , Homologia de Sequência do Ácido NucleicoRESUMO
The locus Om (ovum mutant) identified in the mouse strain DDK affects the viability of (DDK x non-DDK)F1 preimplantation embryos. We previously located this locus on Chromosome (Chr) 11 close to Scya2 (Baldacci et al. Mamm. Genome 2, 100-105, 1992). Here we report a high-resolution map of the region around Om based on a large number of backcross individuals. The same region has been analyzed on the EUCIB backcross, and the two maps have been compared. The results define the proximal and distal boundaries for the Om mutation as Scya2 and D11Mit36 respectively. The distance between these two markers is about 2 cM. These data should facilitate the positional cloning and molecular characterization of Om.
Assuntos
Mapeamento Cromossômico , Camundongos Endogâmicos , Animais , Sequência de Bases , Cruzamentos Genéticos , Primers do DNA , Feminino , Marcadores Genéticos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Dados de Sequência Molecular , Óvulo , Recombinação GenéticaAssuntos
Proteínas Cromossômicas não Histona , Mapeamento Cromossômico , Cromossomos , Drosophila/genética , Heterocromatina , Proteínas de Insetos , Camundongos/genética , Proteínas/genética , Homologia de Sequência do Ácido Nucleico , Alelos , Animais , Sequência de Bases , Sequência Conservada , Feminino , Masculino , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Mutantes , Dados de Sequência MolecularRESUMO
The DDK inbred strain of mouse has a striking particularity: when DDK females are crossed to males of other strains they exhibit a reduced fertility, whereas the reciprocal crosses (non-DDK females x DDK males) are fertile (Wakasugi et al. 1967; Wakasugi 1973). The low fertility results from an early embryonic lethality, the F1 embryos dying near the late morula-early blastocyst stage. Genetic analyses (Wakasugi 1974) and nuclear and cytoplasmic transfers (Renard and Babinet 1986; Babinet et al. 1990; Mann 1986), have shown that the failure of the embroys to develop is due to an incompatibility between a DDK maternally encoded cytoplasmic product and the non-DDK paternal genome. In order to elucidate the genetic determinism of this embryonic lethality, we have analyzed the fertility of male progeny from a backcross BALB/c females x (BALB/c x DDK)F1 males and that of males from a set of recombinant inbred (RI) strains, established from DDK and BALB/c progenitors, when mated with DDK females. Our results indicate that a single locus, Om, is responsible for the DDK syndrome and is located on Chromosome (Chr) 11, very close to the Sigje locus.
Assuntos
Fertilidade/genética , Animais , Southern Blotting , Mapeamento Cromossômico , Cruzamentos Genéticos , DNA Satélite , Feminino , Ligação Genética , Marcadores Genéticos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos , Polimorfismo de Fragmento de Restrição , SíndromeRESUMO
Infection of mouse embryos at 8 days of gestation with a replication-defective retrovirus carrying the human c-Ha-ras-1 oncogene led to efficient and rapid induction of hyperplastic lesions. Twenty-four percent of viable off-spring developed abnormal growths after infection with purified virus. The lesions contained a single integrated provirus and produced viral RNA and the Ha-ras oncogene product (p21). The latency period between the time of infection and appearance of the lesions suggested that secondary alterations in addition to activated ras were necessary for neoplasms to develop. The earliest and most abundant growths were cutaneous and appeared from 4 to 36 weeks of age, with a median of 4 weeks of age. A number of subcutaneous lesions also developed over the same time span but at a median of 18 weeks of age. The rapid development of cutaneous lesions in response to transduction of the ras oncogene contrasts with other studies in which adult skin required secondary treatment with promoters prior to ras induction of epithelial hyperplasia. These results demonstrate that infection of midgestation mouse embryos allows rapid analysis of oncogene potency in skin.
