scholarly journals Transcriptional Bursting and Co-bursting Regulation by Steroid Hormone Release Pattern and Transcription Factor Mobility

2019 ◽  
Vol 75 (6) ◽  
pp. 1161-1177.e11 ◽  
Author(s):  
Diana A. Stavreva ◽  
David A. Garcia ◽  
Gregory Fettweis ◽  
Prabhakar R. Gudla ◽  
George F. Zaki ◽  
...  
2021 ◽  
Author(s):  
Liang Ma ◽  
Zeyue Gao ◽  
Jiegen Wu ◽  
Bijunyao Zhong ◽  
Yuchen Xie ◽  
...  

2021 ◽  
Author(s):  
Ineke Brouwer ◽  
Emma Kerklingh ◽  
Fred van Leeuwen ◽  
Tineke L Lenstra

Transcriptional bursting has been linked to the stochastic positioning of nucleosomes. However, how bursting is regulated by remodeling of promoter nucleosomes is unknown. Here, we use single-molecule live-cell imaging of GAL10 transcription in budding yeast to measure how transcriptional bursting changes upon single and double perturbations of chromatin remodeling factors, the transcription factor Gal4 and preinitiation complex (PIC) components. Using dynamic epistasis analysis, we reveal how remodeling of different nucleosomes regulates individual transcriptional bursting parameters. At the nucleosome covering the Gal4 binding sites, RSC acts synergistically with Gal4 binding to facilitate each burst. Conversely, nucleosome remodeling at the TATA box controls only the first burst upon galactose induction. In the absence of remodelers, nucleosomes at canonical TATA boxes are displaced by TBP binding to allow for transcription activation. Overall, our results reveal how promoter nucleosome remodeling, together with transcription factor and PIC binding regulates the kinetics of transcriptional bursting.


2007 ◽  
Vol 176 (6) ◽  
pp. 843-852 ◽  
Author(s):  
Chike Cao ◽  
Yanling Liu ◽  
Michael Lehmann

Cell death during Drosophila melanogaster metamorphosis is controlled by the steroid hormone 20-hydroxyecdysone (20E). Elements of the signaling pathway that triggers death are known, but it is not known why some tissues, and not others, die in response to a particular hormone pulse. We found that loss of the tissue-specific transcription factor Fork head (Fkh) is both required and sufficient to specify a death response to 20E in the larval salivary glands. Loss of fkh itself is a steroid-controlled event that is mediated by the 20E-induced BR-C gene, and that renders the key death regulators hid and reaper hormone responsive. These results implicate the D. melanogaster FOXA orthologue Fkh with a novel function as a competence factor for steroid-controlled cell death. They explain how a specific tissue is singled out for death, and why this tissue survives earlier hormone pulses. More generally, they suggest that cell identity factors like Fkh play a pivotal role in the normal control of developmental cell death.


2012 ◽  
Vol 21 (3) ◽  
pp. 283-295 ◽  
Author(s):  
U. Gangishetti ◽  
J. Veerkamp ◽  
D. Bezdan ◽  
H. Schwarz ◽  
I. Lohmann ◽  
...  

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