GERM-CELL NUCLEAR ANTIGEN (GCNA1) EXPRESSION DOES NOT REQUIRE A GONADAL ENVIRONMENT OR STEROIDOGENIC FACTOR-1 - EXAMINATION OF GCNA1 IN ECTOPIC GERM-CELLS AND IN FTZ-F1 NULL MICE

The germ cell lineage is first recognized as a population of mitotical ly proliferating primordial germ cells that migrate toward the gonadal ridge. Shortly after arriving at the gonadal ridge, the germ cells be gin to initiate a commitment to gamete production in the developing go nad, The mechanisms controlling this transition are poorly understood. We recently reported that a mouse germ cell nuclear antigen 1 (GCNA1) is initially detected in both male and female germ cells as they reac h the gonad at 11.5 days postcoitum (dpc), GCNA1 is continually expres sed in germ cells through all stages of gametogenesis until the diplot ene/dictyate stage of meiosis I. Since GCNA1 expression commences soon after primordial germ cells arrive at the gonadal ridge, we wanted to determine whether the gonadal environment was essential for induction of GCNA1 expression. By examining GCNA1 expression in germ cells that migrate ectopically into the adrenal gland, we determined that both t he gonadal and adrenal gland environments allow GCNA1 expression. We a lso examined GCNA1 expression in Ftz-F1 null mice, which are born lack ing gonads and adrenal glands. During embryonic development in the Ftz -F1 null mice, the gonad and most germ cells undergo apoptotic degener ation at about 12.5 dpc. While most of the germ cells undergo apoptosi s without expressing GCNA1, a few surviving germs cells, especially ou tside the involuting gonad clearly express GCNA1. Thus, although the F tz-F1 gene is essential for gonadal and adrenal development, induction of GCNA1 expression in germ cells does not require Ftz-F1 gene produc ts. The finding that germ cell GCNA1 expression is not restricted to t he gonadal environment and is not dependent on the Ftz-F1 gene product s suggests that GCNA1 expression may be initiated in the germ cell lin eage by autonomous means. (C) 1997 Wiley-Liss, Inc.