scholarly journals BAX regulates follicular endowment in mice

Reproduction ◽  
2007 ◽  
Vol 133 (5) ◽  
pp. 865-876 ◽  
Author(s):  
Chuck R Greenfeld ◽  
Melissa E Pepling ◽  
Janice K Babus ◽  
Priscilla A Furth ◽  
Jodi A Flaws

It is believed that the endowment of primordial follicles in mammalian ovaries is finite. Once follicles are depleted, infertility ensues. Thus, the size of the initial endowment has consequences for fertility and reproductive longevity. Follicular endowment is comprised of various processes that culminate with the incorporation of meiosis-arrested oocytes into primordial follicles. Apoptosis is prominent during follicular endowment, and apoptosis regulatory genes are involved in its regulation. Conflicting data exist with regard to the role of the proapoptotic Bcl-2 associated X protein (BAX) in follicular endowment. Therefore, we investigated the role of BAX during follicular endowment in embryonic and neonatal ovaries. We found that BAX is involved in regulating follicular endowment in mice. Deletion ofBaxyields increased oocyte numbers in embryonic ovaries and increased follicle numbers in neonatal ovaries when compared with wild-type ovaries. Increased follicular endowment inBax−/−ovaries is not due to enhanced germ cell viability. Further, it is not due to an increased primordial germ cell (PGC) allotment, a delay in the onset of meiosis, or altered proliferative activity of oogonia. Instead, our data suggest that the regulatory activity of BAX in follicular endowment likely occurs during PGC migration, prior to PGC colonization of the gonad.

2021 ◽  
Vol 11 (10) ◽  
Author(s):  
Ming‐Yu Zhang ◽  
Yu Tian ◽  
Shu‐Er Zhang ◽  
Hong‐Chen Yan ◽  
Wei Ge ◽  
...  

Andrology ◽  
2013 ◽  
Vol 1 (5) ◽  
pp. 779-786 ◽  
Author(s):  
A. Díez-Torre ◽  
M. Díaz-Núñez ◽  
C. Eguizábal ◽  
U. Silván ◽  
J. Aréchaga

2000 ◽  
Vol 91 (1-2) ◽  
pp. 143-152 ◽  
Author(s):  
Michael R Bendel-Stenzel ◽  
Miranda Gomperts ◽  
Robert Anderson ◽  
Janet Heasman ◽  
Christopher Wylie

Cell Cycle ◽  
2015 ◽  
Vol 14 (19) ◽  
pp. 3016-3029 ◽  
Author(s):  
Rui Sun ◽  
Yuan-Chao Sun ◽  
Wei Ge ◽  
Hui Tan ◽  
Shun-Feng Cheng ◽  
...  

2011 ◽  
Vol 55 (10-11-12) ◽  
pp. 909-916 ◽  
Author(s):  
Chang Liu ◽  
Paichi Tsai ◽  
Ana-Marie García ◽  
Brandon Logeman ◽  
Tetsuya S. Tanaka

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 561-568 ◽  
Author(s):  
M.J. O'Neill ◽  
K. Artzt

The Tctex-1 gene family maps to the t complex of the mouse and consists of four copies on chromosome 17 in both wild-type and t-haplotypes. Tctex-1 mRNA is eightfold overexpressed in male and female germ cells in t-haplotype compound heterozygotes (tx/ty). In order to determine the cause of this aberrant expression and the role of this gene family in spermatogenesis and oogenesis it was subjected to extensive molecular analysis. We find that Tctex-1 protein is present in sperm tails and oocytes and that it is present at equal levels in wild-type and t-haplotype testis. Surprisingly, the excess message in t-haplotypes is not translated. Sequence analysis of the gene family reveals that one copy in t-haplotypes has a mutated start codon. This same copy is deleted for a protein-binding motif in its promoter. This motif, GIM (Germ cell Inhibitory Motif) has strong homology to the Xenopus AP-2-binding site but does not appear to be a binding site for mammalian AP-2. A factor(s) present in testis and ovary, but absent in other mouse tissues binds specifically to this site. Transfection assays using Tctex-1 promoter constructs suggest that GIM functions as a transcriptional repressor. The possible role of Tctex-1 in t complex transmission ratio distortion and sterility is discussed.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Anastasiya Sybirna ◽  
Walfred W. C. Tang ◽  
Merrick Pierson Smela ◽  
Sabine Dietmann ◽  
Wolfram H. Gruhn ◽  
...  

2004 ◽  
Vol 71 (6) ◽  
pp. 1822-1827 ◽  
Author(s):  
Soma Bandyopadhyay ◽  
Sutapa Banerjee ◽  
Alok K. Pal ◽  
Sourendra K. Goswami ◽  
Baidyanath Chakravarty ◽  
...  

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