scholarly journals Promoter decoding of transcription factor dynamics involves a trade‐off between noise and control of gene expression

2013 ◽  
Vol 9 (1) ◽  
pp. 704 ◽  
Author(s):  
Anders S Hansen ◽  
Erin K O'Shea
2016 ◽  
Vol 44 (22) ◽  
pp. 10554-10570 ◽  
Author(s):  
Luke Maishman ◽  
Samson O. Obado ◽  
Sam Alsford ◽  
Jean-Mathieu Bart ◽  
Wei-Ming Chen ◽  
...  

2020 ◽  
Vol 7 (1) ◽  
pp. 191048 ◽  
Author(s):  
Dimple Karia ◽  
Robert C. G. Gilbert ◽  
Antonio J. Biasutto ◽  
Catherine Porcher ◽  
Erika J. Mancini

Chromatin remodelling and transcription factors play important roles in lineage commitment and development through control of gene expression. Activation of selected lineage-specific genes and repression of alternative lineage-affiliated genes result in tightly regulated cell differentiation transcriptional programmes. However, the complex functional and physical interplay between transcription factors and chromatin-modifying enzymes remains elusive. Recent evidence has implicated histone demethylases in normal haematopoietic differentiation as well as in malignant haematopoiesis. Here, we report an interaction between H3K4 demethylase JARID1A and the haematopoietic-specific master transcription proteins SCL and GATA1 in red blood cells. Specifically, we observe a direct physical contact between GATA1 and the second PHD domain of JARID1A. This interaction has potential implications for normal and malignant haematopoiesis.


1995 ◽  
Vol 128 (6) ◽  
pp. 1111-1119 ◽  
Author(s):  
C Rosette ◽  
M Karin

Cell shape changes exert specific effects on gene expression. It has been speculated that the cytoskeleton is responsible for converting changes in the cytoarchitecture to effects on gene transcription. However, the signal transduction pathways responsible for cytoskeletal-nuclear communication remained unknown. We now provide evidence that a variety of agents and conditions that depolymerize microtubules activate the sequence-specific transcription factor NF-kappa B and induce NF kappa B-dependent gene expression. These effects are caused by depolymerization of microtubule because they are blocked by the microtubule-stabilizing agent taxol. In nonstimulated cells, the majority of NF-kappa B resides in the cytosplasm as a complex with its inhibitor I kappa B. Upon cell stimulation, NF-kappa B translocates to the nucleus with concomitant degradation of I kappa B. We show that cold-induced depolymerization of microtubules also leads to I kappa B degradation and activation of NF-kappa B. However, the activated factor remains in the cytoplasm and translocates to the nucleus only upon warming to 37 degrees C, thus revealing two distinct steps in NF-kappa B activation. These findings establish a new role for NF-kappa B in sensing changes in the state of the cytoskeleton and converting them to changes in gene activity.


Sign in / Sign up

Export Citation Format

Share Document