Cutting edge Seminar

 

Speaker:

Yumiko SAGA, Ph.D. (Professor, Mammalian Development Laboratory, NATIONAL INSTITUTE OF GENETICS)

 

Date&Time:  26 Oct. (Wed.) 2016, 12:00- 13:00
Venue: Conference Room(1F), IMEG

Abstract:

In mammals, primordial germ cells (PGCs) that emerge in the early embryo have the capability to become either spermatocytes or oocytes. The fate of PGC is determined after enclosed by somatic cells in embryonic testes or ovaries. In testes, sex-determining region Y (SRY) and its downstream effectors in somatic cells determine the fate of male germ cells. We find that the induction of Nanos2, an RNA binding protein is critical to promote male pathway and Nanos2 works as a male determinant (1-3). In ovaries, WNT signal is implicated in the sex determination of somatic cells. However, it is largely unknown what somatic signals directly regulate the fate of germ cells. Recently, we find that deletion of SMAD4, an effector of BMP signaling, suppresses genes required for follicular formation. Furthermore, female germ cells lacking both Smad4 and Stra8 (a meiosis inducer) develop as male gonocyte-like cells in ovaries, indicating that these two factors work as female germ cell determinants (5). To our surprise, the sexual fate switch observed in the dKO ovary is not accompanied by gene expression changes in somatic cells, revealing the unexpected finding that somatic factors controlled by sex-determining region Y (SRY) are dispensable for the induction of male-specific genes in germ cells.

 

References

1. Suzuki A, Saga Y. Nanos2 suppresses meiosis and promotes male germ cell differentiation. Genes & Develop. 22, 430-435 (2008)
2. Wu Q. et al. SMAD2 and p38 signaling pathways act in concert to determine XY primordial germ cell fate in mice. Development. 142:575-86 (2015)
3. Suzuki A. et al. Dead end1 is an essential partner of NANOS2 for selective binding of target RNAs in male germ cell development. EMBO Rep. 17(1):37-46 (2016)
4. Wu Q. et al. Sexual Fate Change of XX Germ Cells Caused by the Deletion of SMAD4 and STRA8 Independent of Somatic Sex Reprogramming. PLOS Biol. 8:e1002553 (2016)

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