Effect of Optogenetic Stimulus on the Proliferation and Cell Cycle Progression of Neural Stem Cells

2014 ◽  
Vol 247 (6) ◽  
pp. 493-500 ◽  
Author(s):  
Shao Jun Wang ◽  
Chuan Huang Weng ◽  
Hai Wei Xu ◽  
Cong Jian Zhao ◽  
Zheng Qin Yin
PLoS ONE ◽  
2010 ◽  
Vol 5 (12) ◽  
pp. e14203 ◽  
Author(s):  
Yuyoung Joo ◽  
Sungji Ha ◽  
Bo-Hyun Hong ◽  
Jeong a Kim ◽  
Keun-A Chang ◽  
...  

2008 ◽  
Vol 22 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Wenwu Li ◽  
Guoqiang Sun ◽  
Su Yang ◽  
Qiuhao Qu ◽  
Kinichi Nakashima ◽  
...  

Abstract TLX is an orphan nuclear receptor that is expressed exclusively in vertebrate forebrains. Although TLX is known to be expressed in embryonic brains, the mechanism by which it influences neural development remains largely unknown. We show here that TLX is expressed specifically in periventricular neural stem cells in embryonic brains. Significant thinning of neocortex was observed in embryonic d 14.5 TLX-null brains with reduced nestin labeling and decreased cell proliferation in the germinal zone. Cell cycle analysis revealed both prolonged cell cycles and increased cell cycle exit in TLX-null embryonic brains. Increased expression of a cyclin-dependent kinase inhibitor p21 and decreased expression of cyclin D1 provide a molecular basis for the deficiency of cell cycle progression in embryonic brains of TLX-null mice. Furthermore, transient knockdown of TLX by in utero electroporation led to precocious cell cycle exit and differentiation of neural stem cells followed by outward migration. Together these results indicate that TLX plays an important role in neural development by regulating cell cycle progression and exit of neural stem cells in the developing brain.


2010 ◽  
Vol 68 ◽  
pp. e450
Author(s):  
Hee Jin Kim ◽  
Yuyoung Joo ◽  
Bo-Hyun Hong ◽  
Sungji Ha ◽  
Jeong-A Kim ◽  
...  

2010 ◽  
Vol 19 (4) ◽  
pp. 453-460 ◽  
Author(s):  
Peter J. Quesenberry ◽  
Gerri J. Dooner ◽  
Michael Del Tatto ◽  
Gerald A. Colvin ◽  
Kevin Johnson ◽  
...  

2020 ◽  
Vol 25 (6) ◽  
pp. 427-438 ◽  
Author(s):  
Yuhei Yamauchi ◽  
Akihiro Nita ◽  
Masaaki Nishiyama ◽  
Yoshiharu Muto ◽  
Hideyuki Shimizu ◽  
...  

Biomedicines ◽  
2020 ◽  
Vol 8 (10) ◽  
pp. 397
Author(s):  
Cheuk Yiu Tenny Chung ◽  
Paulisally Hau Yi Lo ◽  
Kenneth Ka Ho Lee

BRISC and BRCA1-A complex member 2 (Babam2) plays an essential role in promoting cell cycle progression and preventing cellular senescence. Babam2-deficient fibroblasts show proliferation defect and premature senescence compared with their wild-type (WT) counterpart. Pluripotent mouse embryonic stem cells (mESCs) are known to have unlimited cell proliferation and self-renewal capability without entering cellular senescence. Therefore, studying the role of Babam2 in ESCs would enable us to understand the mechanism of Babam2 in cellular aging, cell cycle regulation, and pluripotency in ESCs. For this study, we generated Babam2 knockout (Babam2−/−) mESCs to investigate the function of Babam2 in mESCs. We demonstrated that the loss of Babam2 in mESCs leads to abnormal G1 phase retention in response to DNA damage induced by gamma irradiation or doxorubicin treatments. Key cell cycle regulators, CDC25A and CDK2, were found to be degraded in Babam2−/− mESCs following gamma irradiation. In addition, Babam2−/− mESCs expressed p53 strongly and significantly longer than in control mESCs, where p53 inhibited Nanog expression and G1/S cell cycle progression. The combined effects significantly reduced developmental pluripotency in Babam2−/− mESCs. In summary, Babam2 maintains cell cycle regulation and pluripotency in mESCs in response to induced DNA damage.


2018 ◽  
Vol 10 (4) ◽  
pp. 1355-1368 ◽  
Author(s):  
Stephanie Chrysanthou ◽  
Claire E. Senner ◽  
Laura Woods ◽  
Elena Fineberg ◽  
Hanneke Okkenhaug ◽  
...  

2015 ◽  
Vol 210 (2) ◽  
pp. 2102OIA144
Author(s):  
Nicole Mende ◽  
Erika E Kuchen ◽  
Mathias Lesche ◽  
Tatyana Grinenko ◽  
Konstantinos D Kokkaliaris ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document