Transmission-ratio distortion through F{sub 1} females at chromosome 11 loci linked to Om in the mouse DDK syndrome
Abstract
We determined the genotypes of >200 offspring that are survivors of matings between female reciprocal F{sub 1} hybrids (between the DDK and C57BL/6J inbred mouse strains) and C57BL/6J males at markers linked to the Ovum mutant (Om) locus on chromosome 11. In contrast to the expectations of our previous genetic model to explain the {open_quotes}DDK syndrome,{close_quotes} the genotypes of these offspring do not reflect preferential survival of individuals that receive C57BL/6J alleles from the F{sub 1} females in the region of chromosome 11 to which the Om locus has been mapped. In face, we observe significant transmission-ratio distortion in favor of DDK alleles in this region. These results are also in contrast to the expectation of Wakasugi`s genetic model for the inheritance of Om, in which he proposed equal transmission of DDK and non-DDK alleles from F{sub 1} females. We propose that the results of these experiments may be explained by reduced expression of the maternal DDK Om allele or expression of the maternal DDK Om allele in only a portion of the ova of F{sub 1} females. 23 refs., 2 figs., 2 tabs.
- Authors:
-
- Temple Univ. School of Medicine, Philadelphia, PA (United States); and others
- Publication Date:
- OSTI Identifier:
- 518189
- Resource Type:
- Journal Article
- Journal Name:
- Genetics
- Additional Journal Information:
- Journal Volume: 142; Journal Issue: 4; Other Information: PBD: Apr 1996
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 55 BIOLOGY AND MEDICINE, BASIC STUDIES; GENES; GENE MUTATIONS; GENETIC MAPPING; GENE REGULATION; LETHAL MUTATIONS; GENETICS; CHROMOSOMES; MICE; HEREDITARY DISEASES; GENOTYPE; PROGENY; OVA; HYBRIDIZATION; PHENOTYPE; BIOLOGICAL MODELS; EMBRYOS; DEATH; FEMALES; BIOLOGICAL MARKERS
Citation Formats
Villena, F P.M. de, Naumova, A K, Smith, M, and Verner, A. Transmission-ratio distortion through F{sub 1} females at chromosome 11 loci linked to Om in the mouse DDK syndrome. United States: N. p., 1996.
Web.
Villena, F P.M. de, Naumova, A K, Smith, M, & Verner, A. Transmission-ratio distortion through F{sub 1} females at chromosome 11 loci linked to Om in the mouse DDK syndrome. United States.
Villena, F P.M. de, Naumova, A K, Smith, M, and Verner, A. 1996.
"Transmission-ratio distortion through F{sub 1} females at chromosome 11 loci linked to Om in the mouse DDK syndrome". United States.
@article{osti_518189,
title = {Transmission-ratio distortion through F{sub 1} females at chromosome 11 loci linked to Om in the mouse DDK syndrome},
author = {Villena, F P.M. de and Naumova, A K and Smith, M and Verner, A},
abstractNote = {We determined the genotypes of >200 offspring that are survivors of matings between female reciprocal F{sub 1} hybrids (between the DDK and C57BL/6J inbred mouse strains) and C57BL/6J males at markers linked to the Ovum mutant (Om) locus on chromosome 11. In contrast to the expectations of our previous genetic model to explain the {open_quotes}DDK syndrome,{close_quotes} the genotypes of these offspring do not reflect preferential survival of individuals that receive C57BL/6J alleles from the F{sub 1} females in the region of chromosome 11 to which the Om locus has been mapped. In face, we observe significant transmission-ratio distortion in favor of DDK alleles in this region. These results are also in contrast to the expectation of Wakasugi`s genetic model for the inheritance of Om, in which he proposed equal transmission of DDK and non-DDK alleles from F{sub 1} females. We propose that the results of these experiments may be explained by reduced expression of the maternal DDK Om allele or expression of the maternal DDK Om allele in only a portion of the ova of F{sub 1} females. 23 refs., 2 figs., 2 tabs.},
doi = {},
url = {https://www.osti.gov/biblio/518189},
journal = {Genetics},
number = 4,
volume = 142,
place = {United States},
year = {Mon Apr 01 00:00:00 EST 1996},
month = {Mon Apr 01 00:00:00 EST 1996}
}