Human Molecular Genetics, 2002, Vol. 11, No. 24 3047-3053
© 2002 Oxford University Press
A novel gene, Pog, is necessary for primordial germ cell proliferation in the mouse and underlies the germ cell deficient mutation, gcd
1Department of Obstetrics and Gynecology and 2Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA, 3University of Texas, MD Anderson Cancer Center, Houston, TX, USA and 4University of Medicine and Dentistry of New Jersey, Piscataway, NJ, USA
Received July 18, 2002; Accepted September 13, 2002
Primordial germ cells (PGCs) are the precursor of the germ cells in adult gonads. They arise extra-gonadally and migrate through somatic tissues to the presumptive genital ridges, where they proliferate and differentiate into oogonia or spermatogonia cells. Abnormalities in this developmental process can cause embryonic depletion of germ cells leading to infertility in the adult. We report here that the mouse gcd (germ cell deficient) mutant phenotype, characterized by reduced numbers of PGCs and adult sterility, is due to reduced PGC proliferation rather than aberrant migration and is caused by the partial deletion of a single novel gene, Pog (proliferation of germ cells). Pog is critical for normal PGC proliferation, starting between 9.5 and 10.25 dpc when germ cells begin to migrate to the developing genital ridge. Deletion of Pog is also accompanied by reduced embryonic body weight and, on some genetic backgrounds, embryonic lethality. Thus, in addition to being necessary for PGC proliferation, Pog may have a wider significance in early embryonic development.
* To whom correspondence should be addressed at: Department of Obstetrics and Gynecology, Baylor College of Medicine, 6550 Fannin Street (#880), Houston, TX 77030, USA. Tel: +1 7137988221; Fax: +1 7137985074; Email: bishop{at}bcm.tmc.edu
The authors wish it to be known that, in their opinion, these two authors should be considered as joint First Authors.
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