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Transcriptional analyses of the Erythrobacter litoralis DSM 8509 general stress response system

ABSTRACT: Transcriptional analyses of the Erythrobacter litoralis DSM 8509 general stress response system

PROVIDER: PRJNA522279 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8571520.fastq.gz	Fastqsanger.gz
	SRR8571530.fastq.gz	Fastqsanger.gz
	SRR8571540.fastq.gz	Fastqsanger.gz
	SRR8571550.fastq.gz	Fastqsanger.gz
	SRR8571560.fastq.gz	Fastqsanger.gz

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Transcriptional analyses of the Erythrobacter litoralis DSM 8509 general stress response system

Project description:We measured steady-state transcript levels in 1) wild-type E. litoralis DSM 8509, 2) a nepR-ecfG deletion strain (ΔnepR-ecfG), 3) a phyR deletion strain (ΔphyR), 4) a lovK-lovR deletion strain (ΔlovKR), and 5) a gsrK-gsrP deletion strain (ΔgsrKΔgsrP) cultivated in constant white light or in constant dark conditions.

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Project description:Extracytoplasmic function (ECF) sigma factors are environmentally responsive transcriptional regulators. In Alphaproteobacteria, ?EcfG activates general stress response (GSR) transcription and protects cells from multiple stressors. A phosphorylation-dependent protein partner switching mechanism, involving HWE/HisKA_2-family histidine kinases, underlies ?EcfG activation. The identity of these sensor kinases and the signals that regulate them remain largely uncharacterized. We have developed the aerobic anoxygenic photoheterotroph (AAP), Erythrobacter litoralis DSM 8509, as a comparative genetic model to investigate GSR. Using this system, we sought to define the role of visible light and a photosensory HWE kinase, LovK, in regulation of GSR transcription. We identified three HWE kinase genes that collectively control GSR: gsrK and lovK are activators, while gsrP is a repressor. In wild-type cells, GSR transcription is activated in the dark and nearly off in the light, and the opposing activities of gsrK and gsrP are sufficient to modulate GSR transcription in response to illumination. In the absence of gsrK and gsrP, lovK alone is sufficient to activate GSR transcription. lovK is a more robust activator in the dark, and light-dependent regulation by LovK requires that its N-terminal LOV domain be photochemically active. Our studies establish a role for visible light and an ensemble of HWE kinases in light-dependent regulation of GSR transcription in E. litoralis.

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