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Publication : Calgizarrin like gene (Cal) deficient mice undergo normal spermatogenesis.

First Author  Mannan AU Year  2003
Journal  Mol Reprod Dev Volume  66
Issue  4 Pages  431-8
PubMed ID  14579419 Mgi Jnum  J:86467
Mgi Id  MGI:2679930 Doi  10.1002/mrd.10367
Citation  Mannan AU, et al. (2003) Calgizarrin like gene (Cal) deficient mice undergo normal spermatogenesis. Mol Reprod Dev 66(4):431-8
abstractText  The murine calgizzarin like gene (Cal) encodes for a calcium binding protein, which belongs to the S100 family of EF-hand proteins. It is specifically expressed in Sertoli cells in the testis and its expression is down-regulated by unknown factor(s) from spermatocytes/spermatids. In this paper, we show by transfection of a fusion protein of green fluorescent protein and Cal protein into NIH3T3 cells, that the expression of Cal is restricted only in the cytoplasm of the cell. A differentially regulated cytoplasmic expression of the Cal in Sertoli cells during mouse development suggests that Cal might play an important role during spermatogenesis. In order to elucidate the function of the Cal protein in the spermatogenesis, we disrupted the Cal locus in mouse by homologous recombination. In our knockout mouse, we deleted exon 2 and exon 3 of the Cal gene and replaced them with a neomycin cassette, which resulted in a complete loss of the Cal transcript. Male and female Cal4+/- and Cal4-/- mice from genetic backgrounds C57BL/6J x 129X1/SvJ hybrid and 129X1/SvJ inbred exhibited normal phenotype and were fertile. An intensive phenotypic analysis showed no gross abnormalities in testis morphology. The lack of the Cal protein also does not affect the parameters of sperm, as they are able to fertilize the oocytes in a competent manner, which is comparable to wild-type sperm. Collectively our results demonstrate that Cal is a nonessential protein and it does not play an important role in mouse spermatogenesis or in process of fertilization.
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