Project description:Membraneless nuclear condensates are an emerging model of transcriptional regulation that involves spatially clustered enhancers and genes forming transcription condensates (TCs). We used a physical isolation approach and DNA/nascent RNA analysis to investigate the global organization of the genome in TCs. Comparative analysis of the two revealed the dynamic nature of the genome, with stable localization of promoters, dynamic recruitment of enhancers, and dynamic export of gene bodies out of TCs upon gene activation. Our findings also suggest that the RNA binding protein FUS undergoes decondensation upon nascent RNA binding, facilitating gene body export out of TCs.
Project description:A multi-layered structure known as the cell envelope separates the controlled interior of Gram-negative bacteria from a fluctuating physical and chemical environment. Transcription of genes that determine cell envelope structure and function is commonly controlled by a class of environmental regulators known as two-component signal transduction systems (TCS), which are comprised of 1) sensor histidine kinases and 2) response regulators. To discover TCS genes that contribute to cell envelope function in the intracellular mammalian pathogen, Brucella ovis, we subjected a comprehensive collection of non-essential TCS mutants to compounds that disrupt cell membranes and the peptidoglycan cell wall. Our screen led to the discovery of three TCS proteins with unusual regulatory properties that coordinately function to confer resistance to cell envelope stress and to support B. ovis replication in the intracellular niche. This tripartite regulatory system consists of the conserved cell envelope regulator, CenR, and a previously uncharacterized TCS, EssRS. The CenR and EssR response regulators bind a shared set of sites on the B. ovis chromosomes to control transcription of an overlapping set of genes with cell envelope functions. CenR directly interacts with EssR and functions to stimulate phosphoryl transfer from the EssS kinase to EssR and control steady-state levels of EssR protein in the cell via a post-transcriptional mechanism. Our data provide evidence for a new mode of TCS cross-regulation in which a non-cognate response regulator both regulates activity and influences cellular levels of a cognate TCS system.
2023-05-30 | GSE229120 | GEO
Project description:TCS removal and identification of active degrading bacteria in heterotrophic denitrification systems with different carbon sources