The Hippo Transducer TAZ Interacts with the SWI/SNF Complex to Regulate Breast Epithelial Lineage Commitment
Name
Gupta_The hippo.pdf
Size
4.48 MB
Format
Adobe PDF
Checksum (MD5)
e63709a7682d831c5a0de713201473d1
Author(s)
Skibinski, Adam
Breindel, Jerrica L.
Prat, Aleix
Smith, Elizabeth
Rolfs, Andreas
LaBaer, Joshua
Kuperwasser, Charlotte
Galvan, Patricia
Gupta, Piyush
Date Issued
March 2014
Journal
Cell Reports
Publisher
Elsevier
Citation
Skibinski, Adam, Jerrica L. Breindel, Aleix Prat, Patricia Galvan, Elizabeth Smith, Andreas Rolfs, Piyush B. Gupta, Joshua LaBaer, and Charlotte Kuperwasser. “The Hippo Transducer TAZ Interacts with the SWI/SNF Complex to Regulate Breast Epithelial Lineage Commitment.” Cell Reports 6, no. 6 (March 2014): 1059–1072.
Version
Final published version
Abstract
Lineage-committed cells of many tissues exhibit substantial plasticity in contexts such as wound healing and tumorigenesis, but the regulation of this process is not well understood. We identified the Hippo transducer WWTR1/TAZ in a screen of transcription factors that are able to prompt lineage switching of mammary epithelial cells. Forced expression of TAZ in luminal cells induces them to adopt basal characteristics, and depletion of TAZ in basal and/or myoepithelial cells leads to luminal differentiation. In human and mouse tissues, TAZ is active only in basal cells and is critical for basal cell maintenance during homeostasis. Accordingly, loss of TAZ affects mammary gland development, leading to an imbalance of luminal and basal populations as well as branching defects. Mechanistically, TAZ interacts with components of the SWI/SNF complex to modulate lineage-specific gene expression. Collectively, these findings uncover a new role for Hippo signaling in the determination of lineage identity through recruitment of chromatin-remodeling complexes.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Whitehead Institute for Biomedical Research
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1016/j.celrep.2014.02.038
