TEMPORAL PATTERNS OF A-MYB AND B-MYB GENE-EXPRESSION DURING TESTIS DEVELOPMENT

Citation
Ke. Latham et al., TEMPORAL PATTERNS OF A-MYB AND B-MYB GENE-EXPRESSION DURING TESTIS DEVELOPMENT, Oncogene, 13(6), 1996, pp. 1161-1168
Citations number
32
Categorie Soggetti
Oncology,Biology,"Cell Biology
Journal title
ISSN journal
09509232
Volume
13
Issue
6
Year of publication
1996
Pages
1161 - 1168
Database
ISI
SICI code
0950-9232(1996)13:6<1161:TPOAAB>2.0.ZU;2-E
Abstract
We recently reported the cloning and sequencing of the mouse A-myb pro to-oncogene cDNA and the abundant expression of this mRNA primarily in the testis of adult mice. The A-myb mRNA is detectable by in situ hyb ridization specifically in the spermatogenic cells, and is downregulat ed during terminal differentiation. A low level of expression is obser ved in a few other tissues, including ovary, spleen and brain. We have extended those studies by examining A-myb and B-myb expression during testis development in the mouse. The A-myb and B-myb genes are both e xpressed in a cell- and stage-specific manner during testis developmen t. The B-myb mRNA is expressed most highly in gonocytes of the fetal t estis and in spermatogonia and early spermatocytes in the adult. B-myb expression decreases at day 18 post partum, coincident with the initi al appearance of Late pachytene spermatocytes. B-myb expression was al so detectable in some interstitial cells of the fetal and adult testis . The A-myb mRNA was not detectable by in situ hybridization in fetal day 15.5 gonocytes but was detectable at a low abundance by RT-PCR in fetal and newborn mice. A-myb mRNA expression increased at post-natal day 10, when primary spermatocytes first appear. In the adult, the A-m yb mRNA was expressed highly in a sub-population of spermatogonia and in primary spermatocytes, but was not detectable in spermatids. This e xpression of A-myb is consistent with the meiotic arrest that is obser ved in A-myb-deficient male mice. We conclude that B-myb may play a cr itical role in controlling the proliferation or differentiation of gon ocytes and spermatogonia and possibly the somatic lineages as well, wh ereas A-myb is required for progression through the first meiotic prop hase. These distinct roles for B-myb and A-myb during spermatogenesis may reflect distinct transactivation potentials of the two proteins. F urther studies to determine the functions of A-myb and B-myb in the de veloping testis should improve our understanding of the molecular even ts associated with spermatogenesis and differentiation of the Sertoli and other somatic cell types of the testis.