ArticleGenetics2004
Oligosyndactylism mice have an inversion of chromosome 8.
Article in Genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Pathogenesis and potential therapeutic targets of trichorhinophalangeal syndrome; lessons obtained from animal studies.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Review
- Genetic analyses using chromosomal microarray and exome sequencing in fetuses and women with Müllerian duct anomalies.Journal of assisted reproduction and genetics · 2025Article
- Kidney Injury by Unilateral Ureteral Obstruction in Mice Lacks Sex Differences.Kidney & blood pressure research · 2024Article
- Widespread Impact of Chromosomal Inversions on Gene Expression Uncovers Robustness via Phenotypic Buffering.Molecular biology and evolution · 2016Article
- Phenotyping by magnetic resonance imaging nondestructively measures glomerular number and volume distribution in mice with and without nephron reduction.Kidney international · 2016Article
- Sequence characterization and promoter identification of porcine APC10 gene.Molecular biology reports · 2010Article
- Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF.Laboratory investigation; a journal of technical methods and pathology · 2010Article
- Characterization of chromosomal inversion of the mouse hairy ears (Eh) mutation associated with cleft palate.Mammalian genome : official journal of the International Mammalian Genome Society · 2007Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The radiation-induced mutation Oligosyndactylism (Os) is associated with limb and kidney defects in heterozygotes and with mitotic arrest and embryonic lethality in homozygotes. We reported that the cell cycle block in Os and in the 94-A/K transgene-induced mutations is due to disruption of the Anapc10 (Apc10/Doc1) gene. To understand the genetic basis of the limb and kidney abnormalities in Os mice we characterized the structural changes of chromosome 8 associated with this mutation. We demonstrate that the Os chromosome 8 has suffered two breaks that are 5 cM ( approximately 10 Mb) apart and the internal fragment delineated by the breaks is in an inverted orientation on the mutant chromosome. While sequences in proximity to the distal break are present in an abnormal Os-specific Anapc10 hybrid transcript, transcription of these sequences in normal mice is low and difficult to detect. Transfer of the Os mutation onto an FVB/N background indicated that the absence of dominant effects in 94-A/K mice is not due to strain background effects on the mutation. Further analysis of this mutation will determine if a gene interrupted by the break or a long-range effect of the rearrangement on neighboring genes is responsible for the dominant effects of Os.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.