While a number of mouse mutants generated by targeting specific pathways involving hair follicle cycle resulted in nude mice or models of inflammatory alopecia [4], [17], [18], the CRF-OE mouse has not been examined so far as a model relevant to chronic stress-induced alopecia, despite an initial report that CRF-OE mice develop bilateral symmetric hair loss in adulthood [11].
These mouse mutants, one generated by my laboratory, were resistant to cancer, yet had significantlyshortened longevity accompanied by a number of premature aging phenotypes.
Three Tecta mouse mutants were generated by homologous recombination in ES cells that correspond to the human mutations: c.4856G>C (p.C1619S); c.5458C>T, c.5471G>A (p.L1820F, p.G1824D); and c.5509T>G p.C1837GG).
Most mouse (Mus musculus) mutants generated in laboratories have been designed to aid the study of human genetics, physiology or diseases progression.
In summary, Tex19.1−/− mouse mutant that we generated confirms the spermatogenic phenotypes of a previously reported Tex19.1 mutant [15].
One possible explanation for the discrepancy between our mice and other reported mouse models is that BBS mutant mice generated in our laboratory were generated using homologous recombination, while BBS mutant mice that showed PCP defects were generated by gene-trapping methodology.
This synthesis is intended to provide a useful source of reference when studying the molecular controls of hair follicle growth and differentiation, and whenever the hair phenotypes of a newly generated mouse mutant need to be compared with existing ones.
The Ptbp1 mutant mouse generated and analysed here demonstrates how the absence of an RNA-binding protein, involved in splicing and RNA stability among other functions, can completely halt embryonic development.
In conclusion, several Brca1 conventional mouse mutants have been generated that show phenotypic variation, ranging from early embryonic lethality to viable mice that develop tumours.
Until now, a total of 10 different conventional Brca1 mouse mutants have been generated and characterised, each carrying a mutation in a different part of the gene (Xu et al, 1999b; Evers and Jonkers, 2006; Kim et al, 2006).
