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Stationary phase gene regulation by the group A Streptococcus protein RocA

ABSTRACT: We used RNA-Seq to assess how RocA regulates gene expression in stationary phase GAS cultures

ORGANISM(S): Streptococcus pyogenes

PROVIDER: GSE131239 | GEO | 2019/11/22

REPOSITORIES: GEO

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Stationary phase gene regulation in M1 GAS by the group A Streptococcus protein RocA

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Stationary phase gene regulation in M1 GAS by the group A Streptococcus protein RocA

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Stationary phase gene regulation by the group A Streptococcus protein RocA

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Regulation of gene expression in serotype M1 group A Strep (GAS, aka S. pyogenes) by RocA

Project description:We used RNA-Seq to assess whether the rocA gene regulates gene expression in M1 GAS

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Regulatory Rewiring Confers Serotype-Specific Hyper-Virulence in the Human Pathogen Group A Streptococcus

Project description:We sequenced mRNA transcripts from three isogenic M3 serotype GAS strains, parental (MGAS10870), complement (10870::rocAM1), and deletion (10870?rocA). There were no significant changes between the parental and revertant strain. Comparison of the parental and complemented strain revealed several virulence factors were up-regulated in the parental strain where RocA function was diminished. We concluded that RocA, through direct or indirect mechanisms, is able to control numerous virulence genes and this lack of RocA regulation increases expression of virulence factors, which contributes to the hyper-virulent state of serotype M3 GAS. GAS strains were grown to mid-exponential phase, total RNA isolated, rRNA depleted, cDNA libraries synthesized, and libraries analyzed using Illumina MiSeq and CLC Genomics Workbench version 7.5.1 RNA-seq software.

2015-08-24 | E-GEOD-68277 | biostudies-arrayexpress

Regulatory Rewiring Confers Serotype-Specific Hyper-Virulence in the Human Pathogen Group A Streptococcus

Project description:We sequenced mRNA transcripts from three isogenic M3 serotype GAS strains, parental (MGAS10870), complement (10870::rocAM1), and deletion (10870ΔrocA). There were no significant changes between the parental and revertant strain. Comparison of the parental and complemented strain revealed several virulence factors were up-regulated in the parental strain where RocA function was diminished. We concluded that RocA, through direct or indirect mechanisms, is able to control numerous virulence genes and this lack of RocA regulation increases expression of virulence factors, which contributes to the hyper-virulent state of serotype M3 GAS.

2015-08-24 | GSE68277 | GEO

Polymorphisms in RocA contribute to the molecular pathogenesis of serotype M28 group A streptococcus

Project description:RNA-seq experiments of serotype M28 group A streptococcus strains with mutations in rocA at two time points

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RocA has serotype-specific gene regulatory and pathogenesis activity in serotype M28 group A streptococcus

Project description:RNA-seq experiments of a wild-type and isogenic rocA deletion mutant serotype M28 group A streptococcus strain at two time points

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Oxidative stress in stationary-phase cultures

Project description:Background: As carbon sources are exhausted, Saccharomyces cerevisiae cells exhibit reduced metabolic activity and cultures enter stationary phase. We asked whether cells in stationary-phase cultures respond to additional stress at the level of transcript abundance. Results: Microarrays were used to quantify changes in transcript abundance in cells from stationary-phase cultures. In response to oxidative stress, more than 800 mRNAs increased within 1 minute. A significant number of these mRNAs encode proteins involved in stress responses. We tested whether mRNA increases were due to new transcription, rapid poly-adenylation of message (which would not be detected by microarrays), or potential release of mature mRNA sequestered in the cell but insoluble during RNA isolation. Examination of the response to oxidative stress in an RNA polymerase II mutant, rpb1-1 suggested new transcription was not required. Quantitative RT-PCR analysis of a subset of these transcripts further suggested that essentially all isolated transcripts were polyadenylated. In contrast, over 1000 transcripts increased after protease treatment of cell-free lysates from stationary-phase but not exponentially growing cultures. We also determined that oxidative stress and temperature upshift led to the release of different transcripts, suggesting that mRNA release is stress specific. Conclusions: A large number of mRNAs are sequestered in a protease-labile, rapidly releasable form in cells in stationary-phase cultures but not exponentially growing cultures. The differences between mRNAs released by protease treatment and those observed with oxidative stress and temperature upshift, suggest different stresses cause the release of different transcripts. We hypothesize that P-bodies are involved in this sequestration. Keywords: stress response

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