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Protein tyrosine kinase 2 beta (PTK2B), but not focal adhesion kinase (FAK), is expressed in a sexually dimorphic pattern in developing mouse gonads
Author(s) -
Beverdam Annemiek,
Svingen Terje,
BagheriFam Stefan,
McClive Peter,
Sinclair Andrew H.,
Harley Vincent R.,
Koopman Peter
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22396
Subject(s) - biology , microbiology and biotechnology , focal adhesion , sertoli cell , ptk2 , tyrosine kinase , signal transduction , receptor tyrosine kinase , kinase , protein kinase a , medicine , endocrinology , spermatogenesis , mitogen activated protein kinase kinase
Sexual reproduction is essential for the propagation and the maintenance of fitness of our species, and is dependent on the correct development of the bipotential genital ridges into testes and ovaries. Although several transcription factors, secreted signaling molecules, and their receptors have been found to be important for testis determination and early gonad development, comparatively little research has been carried out into intracellular signal transduction pathways activated during these processes. Focal adhesion kinase (FAK) and protein tyrosine kinase 2 beta (PTK2B) form one group of cytosolic tyrosine kinases that are known to be important for processes such as cell proliferation, differentiation, and motility. Here, we describe the temporal and spatial expression patterns of Fak and Ptk2b mRNA and protein during sex determination and early gonadogenesis in mouse embryos. Ptk2b mRNA and PTK2B protein were expressed in testes from 11.5 days post coitum onward, predominantly in developing Sertoli cells, in a SOX9‐dependent manner. Fak mRNA and FAK protein were expressed in gonads of both sexes at all stages examined. Our data suggest cell type‐ and stage‐specific roles for PTK2B during early testis development. Developmental Dynamics 239:2735–2741, 2010. © 2010 Wiley‐Liss, Inc.