scholarly journals High telomerase is a hallmark of undifferentiated spermatogonia and is required for maintenance of male germline stem cells

2015 ◽  
Vol 29 (23) ◽  
pp. 2420-2434 ◽  
Author(s):  
Matthew F. Pech ◽  
Alina Garbuzov ◽  
Kazuteru Hasegawa ◽  
Meena Sukhwani ◽  
Ruixuan J. Zhang ◽  
...  
2003 ◽  
Vol 68 (5) ◽  
pp. 1801-1807 ◽  
Author(s):  
Mito Kanatsu-Shinohara ◽  
Shinya Toyokuni ◽  
Takeshi Morimoto ◽  
Shigeyuki Matsui ◽  
Tasuku Honjo ◽  
...  

2006 ◽  
Vol 74 (3) ◽  
pp. 522-529 ◽  
Author(s):  
Mito Kanatsu-Shinohara ◽  
Kimiko Inoue ◽  
Jiyoung Lee ◽  
Hiromi Miki ◽  
Narumi Ogonuki ◽  
...  

2012 ◽  
Vol 23 (8) ◽  
pp. 1524-1532 ◽  
Author(s):  
Therese M. Roth ◽  
C.-Y. Ason Chiang ◽  
Mayu Inaba ◽  
Hebao Yuan ◽  
Viktoria Salzmann ◽  
...  

Drosophila male germline stem cells (GSCs) divide asymmetrically, balancing self-renewal and differentiation. Although asymmetric stem cell division balances between self-renewal and differentiation, it does not dictate how frequently differentiating cells must be produced. In male GSCs, asymmetric GSC division is achieved by stereotyped positioning of the centrosome with respect to the stem cell niche. Recently we showed that the centrosome orientation checkpoint monitors the correct centrosome orientation to ensure an asymmetric outcome of the GSC division. When GSC centrosomes are not correctly oriented with respect to the niche, GSC cell cycle is arrested/delayed until the correct centrosome orientation is reacquired. Here we show that induction of centrosome misorientation upon culture in poor nutrient conditions mediates slowing of GSC cell proliferation via activation of the centrosome orientation checkpoint. Consistently, inactivation of the centrosome orientation checkpoint leads to lack of cell cycle slowdown even under poor nutrient conditions. We propose that centrosome misorientation serves as a mediator that transduces nutrient information into stem cell proliferation, providing a previously unappreciated mechanism of stem cell regulation in response to nutrient conditions.


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