Sexual dimorphism is common throughout the animal kingdom, with males and females exhibit phenotypic characters specific for their sex. While a great deal is known about the establishment of sexual identity in somatic cells, this process is much less well understood in the germline. Germline sexual identity is critical for sex-specific development of germline stem cells and production of sperm vs. eggs. Thus, it is an essential aspect of animal sexual reproduction and human fertility. Germ cells depend on both signals from the somatic gonad as well as their own sex chromosome genotype to determine their sex. Therefore, when the “sex” the germline fails to match the “sex” of the soma, germline development is severely disrupted. How somatic signals and germ cell intrinsic cues act together to regulate germline sex determination is a key question about which little is known in any organism. We have previously identified the JAK/STAT pathway as a key male determining signal from the soma to the germline; evidence exists for a similar signal in females, but this signal has not been identified. Further, the RNA-binding protein Sex-Lethal (SXL) and the chromatin factor PHF7 have been identified as key components promoting female vs. male germline identity, respectively. We propose that the JAK/STAT pathway is a direct activator of PHF7 expression in the male germline, and that this pathway is inhibited by SXL in the female germline. Further, male-specific expression of PHF7 appears to be regulated at the levels of both transcription and translation to ensure its proper male-specific expression. Additionally we have evidence suggesting signals from the soma can affect PHF7 function, whereas SXL function in the germline seems to be exclusively regulated by intrinsic factors. We are investigating the regulation of the key germline sex determination factors PHF7 and SXL and how they are controlled by both somatic signals and germ cell intrinsic factors.