Premium
Integrin‐FAK‐CDC42‐PP1A signaling gnaws at YAP/TAZ activity to control incisor stem cells
Author(s) -
HicksBerthet Julia,
Varelas Xaralabos
Publication year - 2017
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.201700116
Subject(s) - microbiology and biotechnology , stem cell , hippo signaling pathway , biology , integrin , cdc42 , signal transduction , mtorc1 , mediator , effector , cell , pi3k/akt/mtor pathway , genetics
How epithelial tissues are able to self‐renew to maintain homeostasis and regenerate in response to injury remains a persistent question. The transcriptional effectors YAP and TAZ are increasingly being recognized as central mediators of epithelial stem cell biology, and a wealth of recent studies have been directed at understanding the control and activity of these factors. Recent work by Hu et al. [1][Hu JK, 2017] has added to this knowledge, as they identify an Integrin‐FAK‐CDC42‐PP1A signaling cascade that directs nuclear YAP/TAZ activity in stem cell populations of the mouse incisor, and define convergence on mTORC1 signaling as an important mediator of the proliferation of these cells. Here, we review recent studies on YAP/TAZ function and regulation in epithelial tissue‐specific stem cells, merging the Hu et al. study together with our current knowledge of YAP/TAZ.