Nature Communications (Apr 2019)
MKL1-actin pathway restricts chromatin accessibility and prevents mature pluripotency activation
- Xiao Hu,
- Zongzhi Z. Liu,
- Xinyue Chen,
- Vincent P. Schulz,
- Abhishek Kumar,
- Amaleah A. Hartman,
- Jason Weinstein,
- Jessica F. Johnston,
- Elisa C. Rodriguez,
- Anna E. Eastman,
- Jijun Cheng,
- Liz Min,
- Mei Zhong,
- Christopher Carroll,
- Patrick G. Gallagher,
- Jun Lu,
- Martin Schwartz,
- Megan C. King,
- Diane S. Krause,
- Shangqin Guo
Affiliations
- Xiao Hu
- Department of Cell Biology, Yale University
- Zongzhi Z. Liu
- Department of Cell Biology, Yale University
- Xinyue Chen
- Department of Cell Biology, Yale University
- Vincent P. Schulz
- Department of Pediatrics, Yale University
- Abhishek Kumar
- Department of Medicine (Cardiology), Yale University
- Amaleah A. Hartman
- Department of Cell Biology, Yale University
- Jason Weinstein
- Department of Cell Biology, Yale University
- Jessica F. Johnston
- Department of Cell Biology, Yale University
- Elisa C. Rodriguez
- Department of Cell Biology, Yale University
- Anna E. Eastman
- Department of Cell Biology, Yale University
- Jijun Cheng
- Yale Stem Cell Center, Yale University
- Liz Min
- Department of Cell Biology, Yale University
- Mei Zhong
- Department of Cell Biology, Yale University
- Christopher Carroll
- Department of Cell Biology, Yale University
- Patrick G. Gallagher
- Department of Pathology, Yale Cancer Center, Yale University
- Jun Lu
- Yale Stem Cell Center, Yale University
- Martin Schwartz
- Department of Medicine (Cardiology), Yale University
- Megan C. King
- Department of Cell Biology, Yale University
- Diane S. Krause
- Department of Cell Biology, Yale University
- Shangqin Guo
- Department of Cell Biology, Yale University
- DOI
- https://doi.org/10.1038/s41467-019-09636-6
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 13
Abstract
MKL1 is a key transcriptional co-activator of actin cytoskeleton genes. Here the authors show that MKL1 activation in somatic cells reduces chromatin accessibility and hinders full reprogramming to pluripotency. Reduction of MKL1, disruption of actin cytoskeleton and its links to the nucleus relieve this repression.
