Dataset Information

Identification of sex steroid hormones binding proteins in Pseudomonas aeruginosa.

ABSTRACT: The project aims to elucidate mechanisms driving P. aeruginosa response to sex steroids hormones. An experiment involving Co-immunoprecipitation combined with Mass spectroscopy was performed to identify P. aeruginosa proteins binding to estradiol and /testosterone.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Pseudomonas Aeruginosa Pao1

SUBMITTER: Valerie Yong

LAB HEAD: Sanjay Haresh Chotirmall

PROVIDER: PXD018897 | Pride | 2021-09-09

REPOSITORIES: Pride

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Publications

Sex Steroids Induce Membrane Stress Responses and Virulence Properties in Pseudomonas aeruginosa.

Vidaillac Celine C Yong Valerie Fei Lee VFL Aschtgen Marie-Stephanie MS Qu Jing J Yang Shuowei S Xu Guangfu G Seng Zi Jing ZJ Brown Alexandra C AC Ali Md Khadem MK Jaggi Tavleen K TK Sankaran Jagadish J Foo Yong Hwee YH Righetti Francesco F Nedumaran Anu Maashaa AM Mac Aogáin Micheál M Roizman Dan D Richard Jean-Alexandre JA Rogers Thomas R TR Toyofuku Masanori M Luo Dahai D Loh Edmund E Wohland Thorsten T Czarny Bertrand B Horvat Jay C JC Hansbro Philip M PM Yang Liang L Li Liang L Normark Staffan S Henriques Normark Birgitta B Chotirmall Sanjay H SH

mBio 20200929 5

Estrogen, a major female sex steroid hormone, has been shown to promote the selection of mucoid <i>Pseudomonas aeruginosa</i> in the airways of patients with chronic respiratory diseases, including cystic fibrosis. This results in long-term persistence, poorer clinical outcomes, and limited therapeutic options. In this study, we demonstrate that at physiological concentrations, sex steroids, including testosterone and estriol, induce membrane stress responses in <i>P. aeruginosa</i> This is char ...[more]

PMID: 32994320

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Project description:To advance understanding of mechanisms leading to biological and transcriptional endpoints related to estrogen action in the mouse uterus, we have mapped ERM-NM-1 and RNA polymerase II binding sites using chromatin immunoprecipitation (ChIP) followed by sequencing of enriched chromatin fragments (ChIP-seq). In the absence of hormone, 5184 ERM-NM-1 binding sites were apparent in the vehicle treated ovariectomized uterine chromatin, while 17240 were seen one hour after estrogen (E2) treatment, indicating that some sites are occupied by unliganded ERM-NM-1, and that ERM-NM-1 binding is increased by E2. Approximately 15% of the uterine ERM-NM-1 binding sites were adjacent to (<10 KB) annotated transcription start sites and many sites are found within genes or are found more than 100 KB distal from mapped genes; however, the density (sites per bp) of ERM-NM-1 binding sites is significantly greater adjacent to promoters. An increase in quantity of sites but no significant positional differences were seen between vehicle and E2 treated samples in the overall locations of ERM-NM-1 binding sites either distal from, adjacent to or within genes. Analysis of the PolII data revealed the presence of poised promoter proximal PolII on some highly upregulated genes. Additionally, co-recruitment of PolII and ERM-NM-1 to some distal enhancer regions was observed. A de novo motif analysis of sequences in the ERM-NM-1 bound chromatin confirmed that estrogen response elements (EREs) were significantly enriched. Interestingly, in areas of ERM-NM-1 binding without predicted ERE motifs, homeodomain transcription factor (Hox) binding motifs were significantly enriched. The integration of the ERM-NM-1 and PolII binding sites from our uterine ChIP-seq data with transcriptional responses revealed in our uterine microarrays has the potential to greatly enhance our understanding of mechanisms governing estrogen response in uterine and other estrogen target tissues. one sample each, vehicle ER-alpha ChIP seq,1 hour estradiol ER-alpha ChIP seq, vehicle RNA polymerase II ChIP seq,1 hour estradiol RNA polymerase II ChIP seq, input DNA

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