ArticleMammalian genome : official journal of the International Mammalian Genome Society1993
N-ethyl-N-nitrosourea-induced prenatally lethal mutations define at least two complementation groups within the embryonic ectoderm development (eed) locus in mouse chromosome 7.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 39 citations in OpenAlex.
- Reduced PRC2 function alters male germline epigenetic programming and paternal inheritance.BMC biology · 2018Article
- PRC2 is required for extensive reorganization of H3K27me3 during epigenetic reprogramming in mouse fetal germ cells.Epigenetics & chromatin · 2017Article
- Towards a compendium of essential genes - From model organisms to synthetic lethality in cancer cells.Critical reviews in biochemistry and molecular biology · 2016Review
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- A mono-allelic bivalent chromatin domain controls tissue-specific imprinting at Grb10.The EMBO journal · 2008Article
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- The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.PLoS genetics · 2006Article
- The Polycomb group protein Eed protects the inactive X-chromosome from differentiation-induced reactivation.Nature cell biology · 2006Article
- l7Rn6 encodes a novel protein required for clara cell function in mouse lung development.Genetics · 2006Article
- N-ethyl-N-nitrosourea mutagenesis: boarding the mouse mutant express.Microbiology and molecular biology reviews : MMBR · 2005Review
- Article
- MuTrack: a genome analysis system for large-scale mutagenesis in the mouse.BMC bioinformatics · 2004Review
- Overlapping deletions spanning the proximal two-thirds of the mouse t complex.Mammalian genome : official journal of the International Mammalian Genome Society · 2003Article
- Functional annotation of mammalian genomic DNA sequence by chemical mutagenesis: a fine-structure genetic mutation map of a 1- to 2-cM segment of mouse chromosome 7 corresponding to human chromosome 11p14-p15.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- The Polycomb-group gene eed regulates thymocyte differentiation and suppresses the development of carcinogen-induced T-cell lymphomas.Oncogene · 2002Article
- Article
- A phenotype-based screen for embryonic lethal mutations in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- X-ray-induced mutations in mouse embryonic stem cells.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Complementation analyses for 45 mutations encompassing the pink-eyed dilution (p) locus of the mouse.Genetics · 1995Article
- Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Two loci [l(7)5Rn and l(7)6Rn] defined by N-ethyl-N-nitrosourea (ENU)-induced, prenatally lethal mutations were mapped by means of trans complementation crosses to mice carrying lethal deletions of the albino (c) locus in Chromosome (Chr) 7. Both loci were found to map to the subregion of the Mod-2-sh-1 interval that contains the eed (embryonic ectoderm development) locus, eed has been defined by the inability of embryos homozygous for certain c deletions to develop beyond the early stages of gastrulation. Evidence for at least two loci necessary for normal prenatal development, rather than one locus, that map within the eed interval came from the observation that two prenatally lethal mutations, 3354SB [l(7)5Rn3354SB] and 4234SB [l(7)6Rn4234SB], could complement each other in trans, but could not each be complemented individually by c deletions known to include the eed locus. A somewhat leaky allele of l(7)5Rn [l(7)5Rn1989SB] was also recovered, in which hemizygotes are often stillborn and homozygotes exhibit variable fitness and survival. The mapping of the loci defined by these mutations is likely to be useful for genetic, molecular, and phenotypic characterization of the eed region, and mutations at either locus (or both loci) may contribute to the eed phenotype.
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