ArticleProceedings of the National Academy of Sciences of the United States of America2010
Spontaneous Irs1 passenger mutation linked to a gene-targeted SerpinB2 allele.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
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- Mpeg1 is not essential for antibacterial or antiviral immunity, but is implicated in antigen presentation.Immunology and cell biology · 2022Article
- Identification and characterisation of spontaneous mutations causing deafness from a targeted knockout programme.BMC biology · 2022Article
- Murine SEC24D can substitute functionally for SEC24C during embryonic development.Scientific reports · 2021Article
- Altered phenotype in LMAN1-deficient mice with low levels of residual LMAN1 expression.Blood advances · 2020Article
- Murine Surf4 is essential for early embryonic development.PloS one · 2020Article
- Palmoplantar Keratoderma in Slurp2-Deficient Mice.The Journal of investigative dermatology · 2016Article
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- PON3 knockout mice are susceptible to obesity, gallstone formation, and atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Mammalian COPII coat component SEC24C is required for embryonic development in mice.The Journal of biological chemistry · 2014Article
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- SEC23B is required for the maintenance of murine professional secretory tissues.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Mice deficient in LMAN1 exhibit FV and FVIII deficiencies and liver accumulation of α1-antitrypsin.Blood · 2011Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
In characterizing mice with targeted disruption of the SerpinB2 gene, we observed animals that were small at birth with delayed growth and decreased life expectancy. Although this phenotype cosegregated with homozygosity for the inactive SerpinB2 allele, analysis of homozygous SerpinB2-deficient mice derived from two additional independent embryonic stem (ES) cell clones exhibited no growth abnormalities. Examination of additional progeny from the original SerpinB2-deficient line revealed recombination between the small phenotype (smla) and the SerpinB2 locus. The locus responsible for smla was mapped to a 2.78-Mb interval approximately 30 Mb proximal to SerpinB2, bounded by markers D1Mit382 and D1Mit216. Sequencing of Irs1 identified a nonsense mutation at serine 57 (S57X), resulting in complete loss of IRS1 protein expression. Analysis of ES cell DNA suggests that the S57X Irs1 mutation arose spontaneously in an ES cell subclone during cell culture. Although the smla phenotype is similar to previously reported Irs1 alleles, mice exhibited decreased survival, in contrast to the enhanced longevity reported for IRS1 deficiency generated by gene targeting. This discrepancy could result from differences in strain background, unintended indirect effects of the gene targeting, or the minimal genetic interference of the S57X mutation compared with the conventionally targeted Irs1-KO allele. Spontaneous mutations arising during ES cell culture may be a frequent but underappreciated occurrence. When linked to a targeted allele, such mutations could lead to incorrect assignment of phenotype and may account for a subset of markedly discordant results from experiments independently targeting the same gene.
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