Dataset Information

Heat induction of hsp18 gene expression in Streptomyces albus G: transcriptional and posttranscriptional regulation.

ABSTRACT: In Streptomyces albus G, HSP18, a protein belonging to the small heat shock protein family, could be detected only at high temperature. The nucleotide sequence of the DNA region upstream from hsp18 contains an open reading frame (orfY) which is in the opposite orientation and 150 bp upstream. This open reading frame encodes a basic protein of 225 amino acids showing no significant similarity to any proteins found in data banks. Disruption of this gene in the S. albus chromosome generated mutants that synthesized hsp18 RNA at 30 degrees C, suggesting that orfY plays either a direct or indirect role in the transcriptional regulation of the hsp18 gene. In addition, thermally induced expression of the hsp18 gene is subject to posttranscriptional regulation. In the orfY mutant, although hsp18 RNA was synthesized at a high level at 30 degrees C, the HSP18 protein could not be detected except after heat shock. Synthesis of the HSP18 protein in the orfY mutant was also heat inducible when transcription was inhibited by rifampin. Furthermore, when wild-type cultures of S. albus were shifted from high temperature to 30 degrees C, synthesis of the gene product could no longer be detected, even though large amounts of hsp18 RNA were present.

SUBMITTER: Servant P

PROVIDER: S-EPMC178612 | biostudies-other | 1996 Dec

REPOSITORIES: biostudies-other

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Heat induction of hsp18 gene expression in Streptomyces albus G: transcriptional and posttranscriptional regulation.

Servant P P Mazodier P P

Journal of bacteriology 19961201 24

In Streptomyces albus G, HSP18, a protein belonging to the small heat shock protein family, could be detected only at high temperature. The nucleotide sequence of the DNA region upstream from hsp18 contains an open reading frame (orfY) which is in the opposite orientation and 150 bp upstream. This open reading frame encodes a basic protein of 225 amino acids showing no significant similarity to any proteins found in data banks. Disruption of this gene in the S. albus chromosome generated mutants ...[more]

PMID: 8955381

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Project description:We previously showed that ARHGAP42 is a smooth muscle cell (SMC)-selective, RhoA-specific GTPase activating protein that regulates blood pressure and that a minor allele single nucleotide variation within a DNAse hypersensitive regulatory element in intron1 (Int1DHS) increased ARHGAP42 expression by promoting serum response factor binding. The goal of the current study was to identify additional transcriptional and posttranscriptional mechanisms that control ARHGAP42 expression. Using deletion/mutation, gel shift, and chromatin immunoprecipitation experiments, we showed that recombination signal binding protein for immunoglobulin κ-J region (RBPJ) and TEA domain family member 1 (TEAD1) binding to a conserved core region was required for full IntDHS transcriptional activity. Importantly, overexpression of the notch intracellular domain (NICD) or plating SMCs on recombinant jagged-1 increased IntDHS activity and endogenous ARHGAP42 expression while siRNA-mediated knockdown of TEAD1 inhibited ARHGAP42 mRNA levels. Re-chromatin immunoprecipitation experiments indicated that RBPJ and TEAD1 were bound to the Int1DHS enhancer at the same time, and coimmunoprecipitation assays indicated that these factors interacted physically. Our results also suggest TEAD1 and RBPJ bound cooperatively to the Int1DHS and that the presence of TEAD1 promoted the recruitment of NICD by RBPJ. Finally, we showed that ARHGAP42 expression was inhibited by micro-RNA 505 (miR505) which interacted with the ARHGAP42 3'-untranslated region (UTR) to facilitate its degradation and by AK124326, a long noncoding RNA that overlaps with the ARHGAP42 transcription start site on the opposite DNA strand. Since siRNA-mediated depletion of AK124326 was associated with increased H3K9 acetylation and RNA Pol-II binding at the ARHGAP42 gene, it is likely that AK124326 inhibits ARHGAP42 transcription.NEW & NOTEWORTHY First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.

Dataset Information

Heat induction of hsp18 gene expression in Streptomyces albus G: transcriptional and posttranscriptional regulation.

Publications

Heat induction of hsp18 gene expression in Streptomyces albus G: transcriptional and posttranscriptional regulation.

Similar Datasets

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