ArticleMammalian genome : official journal of the International Mammalian Genome Society2006
Description and genetic mapping of Polypodia: an X-linked dominant mouse mutant with ectopic caudal limbs and other malformations.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Comparison of Gut Microbiological Profiles of Inbred and Outbred Healthy Mice.MicrobiologyOpen · 2025Pooled it
- Comparison of the anesthetic effects of 2,2,2-tribromoethanol on ICR mice derived from three different sources.Laboratory animal research · 2018Article
- Comparison of the response using ICR mice derived from three different sources to multiple low-dose streptozotocin-induced diabetes mellitus.Laboratory animal research · 2017Article
- Annual tendency of research papers used ICR mice as experimental animals in biomedical research fields.Laboratory animal research · 2017Article
- Characterization the response of Korl:ICR mice to loperamide induced constipation.Laboratory animal research · 2016Article
- Comparison of the response using ICR mice derived from three different sources to ethanol/hydrochloric acid-induced gastric injury.Laboratory animal research · 2016Article
- A novel intergenic ETnII-β insertion mutation causes multiple malformations in polypodia mice.PLoS genetics · 2013Article
- Genetic variation and population substructure in outbred CD-1 mice: implications for genome-wide association studies.PloS one · 2009Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
In this report we present a spontaneous mouse mutant, named Polypodia (Ppd), that primarily exhibits ectopic, ventral/caudal limbs and associated pelvic girdle malformation or duplication. Less penetrant features include diphallia, microphthalmia, small kidney, curled or kinked tail, forelimb anomaly, and skin papillae. Ppd mice have a normal karyotype and no large-scale genomic deletions or insertions by BAC-based array comparative genomic hybridization (CGH). Ppd is X-linked dominant with approximately 20% penetrance on the C3H background and maps to X:61.6 Mb-X:71.24 Mb. The limb and a subset of the nonlimb anomalies are similar to those in offspring from retinoic acid-treated dams at E4.5-5.5 and feature overlap with the Disorganization mouse mutant and human patients with ectopic legs. We hypothesize that Ppd affects very early steps in the formation of caudal structures including limb and appendage number. The existence of noncaudal anomalies implies the involvement of Ppd in a broad array of cell fate decisions.
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