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Fetal germ cell development is tightly regulated by the somatic cell environment, and is characterised by cell cycle states that differ between XY and XX gonads. In the testis, gonocytes enter G 1 /G 0  arrest from 12.5 days  post coitum  (dpc) in mice and maintain cell cycle arrest until after birth. Failure to correctly maintain G 1 /G 0  arrest can result in loss of germ cells or, conversely, germ cell tumours. High mobility group box containing transcription factor 1 (HBP1) is a transcription factor that was previously identified in fetal male germ cells at the time of embryonic cell cycle arrest. In somatic cells, HBP1 is classified as a tumour suppressor protein, known to regulate proliferation and senescence. We therefore investigated the possible role of HBP1 in the initiation and maintenance of fetal germ cell G 1 /G 0  arrest using the mouse model. We identified two splice variants of  Hbp1 , both of which are expressed in XY and XX fetal gonads, but only one of which is localised to the nucleus in  in vitro  assays. To investigate  Hbp1  loss of function, we used embryonic stem (ES) cells carrying a Genetrap mutation for  Hbp1  to generate mice lacking Hbp1 function. We found that  Hbp1 -genetrap mouse mutant germ cells proliferated correctly throughout development, and adult males were viable and fertile. Multiple  Hbp1-LacZ  reporter mouse lines were generated, unexpectedly revealing  Hbp1  embryonic expression in hair follicles, eye and limbs. Lastly, in a model of defective germ cell G 1 /G 0  arrest, the  Rb1 -knockout model, we found no evidence for  Hbp1  mis-regulation, suggesting that the reported RB1-HBP1 interaction is not critical in the germline, despite co-expression.

Mice Lacking Hbp1 Function Are Viable and Fertile