Browse by author
Lookup NU author(s): Professor Michael TaggartORCiD, Professor David Elliott
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
The autosomal gene DAZL is a member of a family of genes (DAZL, DAZ, BOULE), all of which contain a consensus RNA binding domain and are expressed in germ cells. Adult male and female mice null for Dazl lack gametes. In order to define more precisely the developmental stages in germ cells that require Dazl expression, the patterns of germ cell loss in immature male and female wild-type (+/+, WT) and Dazl -/- (DazlKO) mice were analysed. In females, loss of germ cells occurred during fetal life and was coincident with progression of cells through meiotic prophase. In males, testes were recovered from WT and DazlKO males obtained before and during the first wave of spermatogenesis (days 2-19). Mitotically active germ cells were present up to and including day 19. Functional differentiation of spermatogonia associated with detection of c-kit positive cells did not depend upon expression of Dazl. RBMY-positive cells (A, intermediate, B spermatogonia, zygotene and preleptotene spermatocytes) were reduced in DazlKO compared with WT testes. Staining of cell squashes from day 19 testes with anti-γ-H2AX and anti-SCP3 antibodies showed that germ cells from DazlKO males were unable to progress beyond the leptotene stage of meiotic prophase I. It was concluded that in the absence of Dazl, germ cells can complete mitosis, and embark on functional differentiation but that, in both sexes, progression through meiotic prophase requires this RNA binding protein.
Author(s): Saunders PTK, Turner JMA, Ruggiu M, Taggart M, Burgoyne PS, Elliott D, Cooke HJ
Publication type: Article
Publication status: Published
Journal: Reproduction
Year: 2003
Volume: 126
Issue: 5
Pages: 589-597
Print publication date: 01/11/2003
ISSN (print): 1470-1626
ISSN (electronic): 1741-7899
Publisher: BioScientifica
URL: http://dx.doi.org/10.1530/rep.0.1260589
DOI: 10.1530/rep.0.1260589
PubMed id: 14611631
Altmetrics provided by Altmetric
