TY - JOUR
T1 - microRNAs selectively protect hub cells of the germline stem cell niche from apoptosis
AU - Volin, Marina
AU - Zohar-Fux, Maayan
AU - Gonen, Oren
AU - Porat-Kuperstein, Lilach
AU - Toledano, Hila
N1 - Publisher Copyright: © 2018 Volin et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
PY - 2018/11/1
Y1 - 2018/11/1
N2 - Genotoxic stress such as irradiation causes a temporary halt in tissue regeneration. The ability to regain regeneration depends on the type of cells that survived the assault. Previous studies showed that this propensity is usually held by the tissue-specific stem cells. However, stem cells cannot maintain their unique properties without the support of their surrounding niche cells. In this study, we show that exposure of Drosophila melanogaster to extremely high levels of irradiation temporarily arrests spermatogenesis and kills half of the stem cells. In marked contrast, the hub cells that constitute a major component of the niche remain completely intact. We further show that this atypical resistance to cell death relies on the expression of certain antiapoptotic microRNAs (miRNAs) that are selectively expressed in the hub and keep the cells inert to apoptotic stress signals. We propose that at the tissue level, protection of a specific group of niche cells from apoptosis underlies ongoing stem cell turnover and tissue regeneration.
AB - Genotoxic stress such as irradiation causes a temporary halt in tissue regeneration. The ability to regain regeneration depends on the type of cells that survived the assault. Previous studies showed that this propensity is usually held by the tissue-specific stem cells. However, stem cells cannot maintain their unique properties without the support of their surrounding niche cells. In this study, we show that exposure of Drosophila melanogaster to extremely high levels of irradiation temporarily arrests spermatogenesis and kills half of the stem cells. In marked contrast, the hub cells that constitute a major component of the niche remain completely intact. We further show that this atypical resistance to cell death relies on the expression of certain antiapoptotic microRNAs (miRNAs) that are selectively expressed in the hub and keep the cells inert to apoptotic stress signals. We propose that at the tissue level, protection of a specific group of niche cells from apoptosis underlies ongoing stem cell turnover and tissue regeneration.
UR - http://www.scopus.com/inward/record.url?scp=85056259049&partnerID=8YFLogxK
U2 - 10.1083/jcb.201711098
DO - 10.1083/jcb.201711098
M3 - Article
C2 - 30093492
SN - 0021-9525
VL - 217
SP - 3829
EP - 3838
JO - Journal of Cell Biology
JF - Journal of Cell Biology
IS - 11
ER -