This Article Full Text Full Text (PDF) All Versions of this Article: 138/5/743    most recent REP-08-0537v1 Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Mithraprabhu, S. Articles by Loveland, K. L PubMed PubMed Citation Articles by Mithraprabhu, S. Articles by Loveland, K. L

Control of KIT signalling in male germ cells: what can we learn from other systems?

¹ Monash Institute for Medical Research, Monash University, Clayton, Victoria 3168, Australia² Australian Research Council Centre of Excellence in Biotechnology and Development, Callaghan, NSW 2308, Australia

Correspondence should be addressed to K L Loveland who is now at Department of Biochemistry and Molecular Biology and Department of Anatomy and Developmental Biology, Monash University, Building 77, Level 1, Wellington Road, Clayton, Victoria 3800, Australia; Email: kate.loveland{at}med.monash.edu.au

The KIT ligand (KITL)/KIT-signalling system is among several pathways known to be essential for fertility. In the postnatal testis, the KIT/KITL interaction is crucial for spermatogonial proliferation, differentiation, survival and subsequent entry into meiosis. Hence, identification of endogenous factors that regulate KIT synthesis is important for understanding the triggers driving germ cell maturation. Although limited information is available regarding local factors in the testicular microenvironment that modulate KIT synthesis at the onset of spermatogenesis, knowledge from other systems could be used as a basis for identifying how KIT function is regulated in germ cells. This review describes the known regulators of KIT, including transcription factors implicated in KIT promoter regulation. In addition, specific downstream outcomes in biological processes that KIT orchestrates are addressed. These are discussed in relationship to current knowledge of mammalian germ cell development.