Genes & cells: Old stem cells lose protective barriers: In young brains, bad proteins confined in newly formed neurons

Science News ◽  
2015 ◽  
Vol 188 (8) ◽  
pp. 10-11
Tina Hesman Saey
2010 ◽  
Vol 30 (6) ◽  
pp. 455-455 ◽  
Dongyan Shi ◽  
Dan Ma ◽  
Feiqing Dong ◽  
Chen Zong ◽  
Liyue Liu ◽  

2010 ◽  
Vol 34 (8) ◽  
pp. S39-S39
Dewu Liu ◽  
Honglan Xiong ◽  
Yuangui Mao ◽  
Peixin Huang ◽  
Jianping Chen ◽  

2010 ◽  
Vol 34 (8) ◽  
pp. S36-S36
Ping Duan ◽  
Xuelin Ren ◽  
Wenhai Yan ◽  
Xuefei Han ◽  
Xu Yan ◽  

2010 ◽  
Vol 34 (8) ◽  
pp. S43-S43
Wei‑ying Zou ◽  
Bei Yang ◽  
Xiuli Ni ◽  
Da‑lei Zhang ◽  
Lei Wu ◽  

2020 ◽  
Vol 64 (2) ◽  
pp. 223-232 ◽  
Ben L. Carty ◽  
Elaine M. Dunleavy

Abstract Asymmetric cell division (ACD) produces daughter cells with separate distinct cell fates and is critical for the development and regulation of multicellular organisms. Epigenetic mechanisms are key players in cell fate determination. Centromeres, epigenetically specified loci defined by the presence of the histone H3-variant, centromere protein A (CENP-A), are essential for chromosome segregation at cell division. ACDs in stem cells and in oocyte meiosis have been proposed to be reliant on centromere integrity for the regulation of the non-random segregation of chromosomes. It has recently been shown that CENP-A is asymmetrically distributed between the centromeres of sister chromatids in male and female Drosophila germline stem cells (GSCs), with more CENP-A on sister chromatids to be segregated to the GSC. This imbalance in centromere strength correlates with the temporal and asymmetric assembly of the mitotic spindle and potentially orientates the cell to allow for biased sister chromatid retention in stem cells. In this essay, we discuss the recent evidence for asymmetric sister centromeres in stem cells. Thereafter, we discuss mechanistic avenues to establish this sister centromere asymmetry and how it ultimately might influence cell fate.

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