|M.Sc Student||Sibony Itzik|
|Subject||Influence of the Mesonephros on the development of the|
indifferent gonad in the chick embryo
|Department||Department of Medicine||Supervisor||Professor Thomas Schultheiss|
|Full Thesis text|
Vertebrate gonads are comprised of two components, the somatic gonad, which forms the bulk of the gonad, and the primordial germ cells (PGC’s), which migrate into the somatic gonad from the outside. The earliest phase in somatic gonad formation is the indifferent gonad phase, in which the gonads are largely indistinguishable between male and female. Although much research has been conducted into sex determination and differentiation of the indifferent gonad into testis or ovary, relatively little is known regarding the specification of the indifferent gonad itself. In particular, the mesonephros (the embryonic kidney), which lies adjacent to the indifferent gonad, plays an important role in development of the testis, but it is not clear whether it also plays a role during indifferent gonad formation. We prevented mesonephros formation in the chick embryo by surgically blocking migration of the nephric duct, which is an essential inducer of the mesonephros. The opposite side of the embryo, where the duct was not blocked, served as a control. Molecular analysis using the mesonephric marker Pax2 confirmed complete absence of the mesonephros on the blocked side. Despite complete inhibition of mesonephros formation, timing of the appearance of the early indifferent gonad markers Lhx9 and Sf1 was not affected, although their spatial expression patterns were somewhat altered, and the germinal epithelium was markedly thinner on the blocked side without any particular apoptosis. Migration of PGC’s into the gonadal epithelium also occurred relatively normally. By HH Stage 26-27, a morphologically identifiable gonad was visible on the blocked side, although it was somewhat smaller than the gonad on the control side. We conclude that the mesonephros is not required for the early stages of indifferent gonad formation, including activation of the molecular markers Lhx9 and Sf1, and for homing of PGC’s to the developing gonad, although it may influence the gonadal growth rate.