Female embryonic lethality in Msh2–Trp53 nullizygous mice is strain dependent

Female embryonic lethality in Msh2–Trp53 nullizygous mice is strain dependent Mammalian Genome 10, 1020–1022 (1999). Incorporating Mouse Genome © Springer-Verlag New York Inc. 1999 Female embryonic lethality in Msh2–Trp53 nullizygous mice is strain dependent Aaron Cranston, Richard Fishel th Genetics and Molecular Biology Program, Kimmel Cancer Center BLSB933, Thomas Jefferson University, 233 South 10 Street, Philadelphia, Pennsylvania 19107, USA Received: 2 April 1999 / Accepted: 8 June 1999 The human DNA mismatch repair (MMR) genes are conserved ments to test the hypothesis that strain differences could account homologs of the Escherichia coli MutHLS system that contribute for the two sets of apparently contradicting data. to genomic instability by surveillance and repair of replication Here, we provide evidence that the difference in the phenotype −/− −/− misincorporation errors and exogenous DNA damage (Fishel and of female Msh2 Trp53 mice observed in these two studies can Wilson 1997). Mutations in one of these MMR genes, hMSH2, be explained by the contribution of different genetic backgrounds account for approximately half of all cases of genetically linked to the genome of these mice. Indeed, the strain dependency of a hereditary non-polyposis colorectal cancer (HNPCC) (Fishel et al. Trp53-related abnormality has been previously reported by Clarke 1993; Nystrom-Lahti et al. 1994). Moreover, p53 is http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Mammalian Genome Springer Journals

Female embryonic lethality in Msh2–Trp53 nullizygous mice is strain dependent

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Publisher
Springer-Verlag
Copyright
Copyright © 1999 by Springer-Verlag New York Inc.
Subject
Life Sciences; Cell Biology; Animal Genetics and Genomics; Human Genetics
ISSN
0938-8990
eISSN
1432-1777
D.O.I.
10.1007/s003359901151
Publisher site
See Article on Publisher Site

Abstract

Mammalian Genome 10, 1020–1022 (1999). Incorporating Mouse Genome © Springer-Verlag New York Inc. 1999 Female embryonic lethality in Msh2–Trp53 nullizygous mice is strain dependent Aaron Cranston, Richard Fishel th Genetics and Molecular Biology Program, Kimmel Cancer Center BLSB933, Thomas Jefferson University, 233 South 10 Street, Philadelphia, Pennsylvania 19107, USA Received: 2 April 1999 / Accepted: 8 June 1999 The human DNA mismatch repair (MMR) genes are conserved ments to test the hypothesis that strain differences could account homologs of the Escherichia coli MutHLS system that contribute for the two sets of apparently contradicting data. to genomic instability by surveillance and repair of replication Here, we provide evidence that the difference in the phenotype −/− −/− misincorporation errors and exogenous DNA damage (Fishel and of female Msh2 Trp53 mice observed in these two studies can Wilson 1997). Mutations in one of these MMR genes, hMSH2, be explained by the contribution of different genetic backgrounds account for approximately half of all cases of genetically linked to the genome of these mice. Indeed, the strain dependency of a hereditary non-polyposis colorectal cancer (HNPCC) (Fishel et al. Trp53-related abnormality has been previously reported by Clarke 1993; Nystrom-Lahti et al. 1994). Moreover, p53 is

Journal

Mammalian GenomeSpringer Journals

Published: Oct 1, 1999

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