PIWI-mediated control of tissue-specific transposons is essential for somatic cell differentiation.
PIWI-mediated control of tissue-specific transposons is essential for somatic cell differentiation.
复制标题
DOI:
10.1016/j.celrep.2021.109776
复制
发表时间:
2021-10-05
期刊:
影响因子:
8.8
通讯作者:
van Wolfswinkel JC
中科院分区:
文献类型:
--
作者:
Li D;Taylor DH;van Wolfswinkel JC
PIWI proteins are known as mediators of transposon silencing in animal germlines but are also found in adult pluripotent stem cells of highly regenerative animals, where they are essential for regeneration. Study of the nuclear PIWI protein SMEDWI-2 in the planarian somatic stem cell system reveals an intricate interplay between transposons and cell differentiation in which a subset of transposons is inevitably activated during cell differentiation, and the PIWI protein is required to regain control. Absence of SMEDWI-2 leads to tissue-specific transposon derepression related to cell-type-specific chromatin remodeling events and in addition causes reduced accessibility of lineage-specific genes and defective cell differentiation, resulting in fatal tissue dysfunction. Finally, we show that additional PIWI proteins provide a stem-cell-specific second layer of protection in planarian neoblasts. These findings reveal a far-reaching role of PIWI proteins and PIWI-interacting RNAs (piRNAs) in stem cell biology and cell differentiation. Chromatin reorganization is an essential part of cell differentiation but risks reactivation of silenced repetitive elements. Li et al. show that planarians use continuous surveillance by a nuclear PIWI protein to chaperone the chromatin transition from pluripotent to differentiated cell, which is crucial for the planarian’s impressive regeneration and homeostasis.
登录
查看更多内容
影响因子:
11.8
作者:
Forsthoefel, David J.;James, Noelle P.;Escobar, David J.;Stary, Joel M.;Vieira, Ana P.;Waters, Forrest A.;Newmark, Phillip A.
通讯作者:
Newmark, Phillip A.
DOI:
10.1093/bioinformatics/btu638
发表时间:
2015-01-15
期刊:
Bioinformatics (Oxford, England)
影响因子:
--
作者:
Anders S;Pyl PT;Huber W
通讯作者:
Huber W
影响因子:
4.9
作者:
Bao W;Kojima KK;Kohany O
通讯作者:
Kohany O
影响因子:
16
作者:
Iwasaki, Yuka W.;Murano, Kensaku;Saito, Kuniaki
通讯作者:
Saito, Kuniaki
影响因子:
4.3
作者:
Bendall, Matthew L.;de Mulder, Miguel;Nixon, Douglas F.
通讯作者:
Nixon, Douglas F.