Journal
TISSUE BARRIERS
Volume 2, Issue 1, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/tisb.28127
Keywords
Amot; Amotl2; Merlin/Nf2; Lats; F-actin; Tead4; Yap; Taz; blastocyst
Categories
Funding
- (KAKENHI) from MEXT [21116003]
- JSPS [23247036, 23770265]
Ask authors/readers for more resources
The Hippo signaling pathway regulates a number of cellular events, including the control of cell fates in preimplantation mouse embryos. The inner and outer cells of the embryo show high and low levels of Hippo signaling, respectively. This position-dependent Hippo signaling promotes the specification of distinct cell fates. In a recent paper, we identified the molecular mechanism that controls Hippo signaling in preimplantation embryos. The junction-associated scaffold protein angiomotin (Amot) plays a key role in this mechanism. At the adherens junctions of the inner cells, Amot activates the Hippo pathway by recruiting and activating the protein kinase large tumor suppressor (Lats). In contrast, Amot at the apical membrane of the outer cells suppresses Hippo signaling by interacting with F-actin. The phosphorylation of Amot inhibits its interaction with F-actin and activates Hippo signaling. We propose that Amot acts as a molecular switch for the Hippo pathway and links F-actin with Lats activity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available