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Redox-sensitive bZIP68 plays a role in balancing stress tolerance with growth in Arabidopsis

ABSTRACT: Redox-sensitive bZIP68 plays a role in balancing stress tolerance with growth in Arabidopsis

PROVIDER: PRJNA552958 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9648610.fastq.gz	Fastqsanger.gz
	SRR9648620_1.fastq.gz	Fastqsanger.gz
	SRR9648620_2.fastq.gz	Fastqsanger.gz
	SRR9648630_1.fastq.gz	Fastqsanger.gz
	SRR9648630_2.fastq.gz	Fastqsanger.gz

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Redox-sensitive bZIP68 plays a role in balancing stress tolerance with growth in Arabidopsis

Project description:Perturbation of the cellular redox state by stress conditions is sensed by redox-sensitive proteins so that the cell can physiologically respond to stressors; however, the mechanisms linking sensing to response remain poorly understood in plants. Here we report that the transcription factor bZIP68 underwent in vivo oxidation in Arabidopsis cells under oxidative stress which is dependent on its redox-sensitive Cys320 residue. bZIP68 is primarily localized to the nucleus under normal conditions in Arabidopsis seedlings and oxidative stress reduces its accumulation in the nucleus and increases its cytosolic localization. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) revealed that bZIP68 primarily binds to promoter regions containing the core G-box (CACGTG) or G-box-like motif of the genes involved in abiotic and biotic stress responses, photosynthesis, biosynthetic processes, and transcriptional regulation. The bzip68 mutant displayed slower growth but enhanced tolerance to oxidative stress. The results from the ChIP-seq and phenotypic and transcriptome comparison between the bzip68 mutant and wildtype indicate that bZIP68 normally suppresses expression of stress tolerance genes and promotes expression of growth-related genes, whereas its inactivation enhances stress tolerance but suppresses growth. bZIP68 might balance stress tolerance with growth through the extent of its oxidative inactivation according to the environment.

2020-07-01 | GSE133900 | GEO

The Mycobacterium tuberculosis Rv2745c Plays an Important Role in Responding to Redox Stress

2014-03-25 | GSE55817 | GEO

The Mycobacterium tuberculosis Rv2745c Plays an Important Role in Responding to Redox Stress

Project description:The Rv2745c (clgR) gene encodes a Clp protease gene regulator that is induced in response to a variety of stress conditions and potentially plays a role in Mtb pathogenesis. The isogenic Mtb:ΔRv2745c mutant is significantly more sensitive to in vitro redox stress generated by diamide, relative to wild-type Mtb, implicating a role for ClgR in the management of intraphagosomal redox stress. Redox stress led to dysregulation of the σH regulon in the isogenic mutant, Mtb:ΔRv2745c. Induction of clgR in Mtb and Mtb:ΔRv2745c (comp) did not lead to Clp protease induction, indicating that clgR has additional functions that need to be elucidated. Disruption of genes involved in sulfate assimilation also occurred in the knock out, implicating clgR as a possible regulator of downstream signaling cascades that facilitate Mtb survival. At different time points, (30, 60 and 90 mins, t=30, t=60 and t=90) following the addition of diamide to M. tuberculosis CDC1551 cultures, RNA was extracted and labeled with Cy5. RNA was also extracted from pre-diamide addition (t=0) time points and labeled with Cy3. These samples were cohybridized on M. tuberculosis CDC1551 whole genome microarrays using biological triplicate samples (i.e. samples derived from three distinct cultures and treatments) and thus three unique datasets were generated for each of the three time points for Mtb. Similar experiments were performed for an isogenic Rv2745c (clgR) mutant in Mtb CDC1551 which was generated by allelic exchange and a complemented strain which was generated by trans-complementation of Rv2745c in the attB locus of the mutant strain, thus restoring the wild type regulation of Rv2745c.

2014-03-25 | E-GEOD-55817 | biostudies-arrayexpress

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Project description:Since oxidative stress plays a major role in liver fibrosis and induces post-translational modifications of proteins, we hypothesized that redox-sensitive HMGB1 isoforms contribute to liver fibrosis progression and resolution. This study is significant because a rise in [H] HMGB1 could flag 'patient at risk', the presence of [O] HMGB1 could suggest 'disease in progress or active scarring', while the appearance of [SO3] HMGB1 could point at 'resolution under way'. The latter could be used as a readout for response to pharmacological intervention with anti-fibrotic agents.

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