Abstract
The mammalian ras gene family encodes key cell-signaling, cell growth-related proteins that have been highly conserved in species from yeast to man. Specific point mutations in the ras genes are associated with various mammalian tumors. To understand the developmental role of the N-ras protooncogene in the mouse, we have disrupted its gene function by homologous recombination in embryonic stem cells. Mice derived from these cells that are homozygous for the N-ras mutation do not produce any detectable N-Ras protein and are morphologically and histologically indistinguishable from their heterozygous and wild-type siblings. Since N-ras is expressed at high levels in hematopoietic cells, we examined different populations of cells in peripheral blood and found no differences between mutant and normal animals. Our results show that N-ras gene function is dispensable for normal mouse development, growth, and fertility.
MeSH Terms
Animals
Base Sequence
Gene Expression Regulation, Developmental
Genes, ras
Heterozygote
Homozygote
Mice
Mice, Knockout
Molecular Sequence Data
Oligodeoxyribonucleotides/chemistry
Proto-Oncogene Proteins p21(ras)/physiology
Restriction Mapping
Chemicals
Oligodeoxyribonucleotides
Proto-Oncogene Proteins p21(ras)
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Umanoff H
Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461.
Edelmann W
Pellicer A
Kucherlapati R
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