RNA-seq of zinc-replete wild type and zinc-limited wild type, altRP operon deletion mutant and its complement strain in Mycolicibacterium (Mycobacterium) smegmatis
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PROVIDER: PRJNA777953 | ENA |
REPOSITORIES: ENA
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Project description:The study was designed to describe the effects of zinc limitation on gene expression in M. smegmatis by comparing the transcriptomes of zinc-replete and zinc-limited wild type. Additionally, the study informs how loss of the altRP operon impacts the transcriptomic changes during zinc limitation by comparing the transcriptomes of zinc-limited ΔaltRP mutant to the zinc-replete and zinc-limited wild type, and to confirm which changes are complemented in the complement strain (ΔaltRP/c).
2021-11-10 | GSE188233 | GEO
Project description:The study was designed to describe the effects of zinc limitation on gene expression in M. smegmatis by comparing the proteomes of zinc-replete and zinc-limited wild type. Additionally, the study informs how loss of the altRP operon impacts the proteome during zinc limitation by comparing the proteomes of zinc-limited ΔaltRP mutant to the zinc-replete and zinc-limited wild type, and to confirm which changes are complemented in the complement strain (ΔaltRP/c).
2021-11-10 | PXD029588 | Pride
Project description:Transcriptomics of Zinc-limited and Zinc-replete Mycobacterium tuberculosis
| PRJNA707587 | ENA
Project description:Purpose: ATG41 is involved both in autophagy and zinc-deficient growth. The goal of this study is to compare transcriptomic profiles of wild-type and atg41Δ strains to discover autophagy-independent molecular phenotypes for the mutant. The atg1Δ mutant is a control for autophagy activity. Methods: Wild-type and mutant yeast were grown to mid-log phase in replete medium and shifted to zinc-deficient medium for 8 hours, after which, cells were harvested for RNA sequencing to detect differential gene expression. Results: Gene expression data for virtually every gene (~6,000) was obtained with ~12,000,000 reads per sample. Differential gene expression analysis showed that several hundred genes were differentially experessed in the atg41Δ mutant (greater than 2-fold) at an FDR of 0.5. Conclusions: Most strikingly, we found that the atg41Δ mutant transcriptome shows signs that sulfur metabolism is distrupted during zinc-deficinet growth. Expression of Met4 gene targets is increased.
2017-12-29 | GSE108603 | GEO
Project description:to analyze the lipidomes of Mycobacterium tuberculosis H37Rv grown in zinc-replete and zinc-limited conditions
2021-03-10 | MSV000087030 | GNPS
Project description:We assessed changes in gene expression in response to zinc availability for the human pathogen Corynebacterium diphtheriae. Expression profiles of wild-type C. diphtheriae strain 1737 grown in semi-defined metal-poor media (mPGT) without and with 5 µM zinc chloride supplementation were compared; the expression profile of wild-type C. diphtheriae strain 1737 in zinc-replete conditions was also compared against an isogenic Δzur mutant grown in zinc-replete conditions. Three biological replicates were prepared by isolating total RNA from mid-logarithmic growth cultures and eleven genes (dip0013, dip0093, dip0173, dip0438, dip1087, dip1486, dip1724, dip2114, dip2128, dip2162, and dip2325) were assessed by real-time PCR to validate the array results. (Abstract) Corynebacterium diphtheriae is a Gram-positive bacterial pathogen and the causative agent of diphtheria, a severe disease of the upper respiratory tract of humans. Factors required for C. diphtheriae to survive in the human host are not well defined, but likely include the acquisition of essential metals such as zinc. In C. diphtheriae, zinc-responsive global gene regulation is controlled by the Zinc Uptake Regulator (Zur), a member of the Fur-family of transcriptional regulators. In this study, we use transcriptomics to identify zinc-regulated genes in C. diphtheriae by comparing gene expression of a wild-type strain grown without and with zinc supplementation. Zur-regulated genes were identified by comparing wild-type gene expression with that of an isogenic zur mutant. We observed zinc repression of several putative surface proteins, the heme efflux system hrtBA, various ABC transporters, and the non-ribosomal peptide synthetase/polyketide synthase cluster sidAB. Furthermore, increased gene expression in response to zinc was observed for the alcohol dehydrogenase, adhA. Zinc and Zur regulation were confirmed for several genes by complementing the zur deletion and subsequent qPCR analysis. We used MEME to predict Zur binding sites within the promoter regions of zinc- and Zur-regulated genes, and verified Zur binding by electrophoretic mobility shift assays. Additionally, we characterized cztA (dip1101), which encodes a putative cobalt/zinc/cadmium efflux family protein. Deletion of cztA results in increased sensitivity to zinc, but not to cobalt or cadmium. This study advances our knowledge of changes to Zur-dependent global gene expression in response to zinc in C. diphtheriae. The identification of zinc-regulated ABC transporters herein will facilitate future studies to characterize zinc transport in C. diphtheriae.
2019-08-15 | GSE131485 | GEO
Project description:Zinc is an essential nutrient because of its role in catalysis and in stabilizing protein structure, but excess zinc can also be deleterious. Four nutritional zinc states have been identified in the alga Chlamydomonas reinhardtii: zinc toxic, zinc replete, zinc deficient and zinc limited. Growth is inhibited in zinc-limited and zinc toxic cells relative to zinc-replete cells, while zinc-deficiency is visually asymptomatic but distinguished by the accumulation of transcripts encoding ZIP family transporters. To identify targets of zinc deficiency and mechanisms of zinc acclimation, we used RNA-seq to probe zinc nutrition responsive changes in gene expression. We identified a subset of genes encoding zinc-handling components, including ZIP family transporters and candidate zinc chaperones. In addition, we noted an impact on two other regulatory pathways, the carbon concentrating mechanism (CCM) and the nutritional copper regulon. Targets of transcription factor Ccm1 and various CAH genes are up-regulated in zinc-deficiency, as a likely consequence of reduced carbonic anhydrase activity, which is validated by mass spectrometry and immunoblot analysis of Cah1, Cah3 and Cah4. Chlamydomonas is therefore not able to grow photoautotrophically in air in zinc limiting conditions, but supplementation with 1% CO2 restores growth to wild-type rates, suggesting that the inability to maintain CCM is a major consequence of zinc limitation. Surprisingly, we noted also that the Crr1 regulon, which responds to Cu limitation, is also turned on in zinc deficiency, and in fact, Crr1 is required for growth in zinc-limiting conditions. Zinc deficient cells are functionally copper deficient, as evidenced by reduced plastocyanin abundance, even though they hyperaccumulate copper up to 50-fold over normal levels. We suggest that zinc-deficient cells sequester Cu in a bio-unavailable form, perhaps to prevent mis-metallation of critical zinc sites. Zn-limited wild-type cells were generated by transfer of cells from the first round of growth in medium with no supplemental Zn into TAP medium supplemented or not with 2.5 µM Zn-EDTA The control samples for this study are represented in GSE25622
2013-05-03 | E-GEOD-41096 | biostudies-arrayexpress
Project description:How cells safeguard essential zinc-dependent functions during zinc deficiency is poorly understood. A long-debated strategy is whether soluble metal-trafficking chaperones exist to prioritize specific zinc-dependent proteins. We identified a eukaryotic family of metallochaperones that physically interacts with zinc-dependent methionine aminopeptidase type I (MAP1) in human and yeast. Deletion of the yeast metallochaperone-encoding gene NMC1 (formerly YNR029c) leads to a zinc-deficiency growth defect and defective initiator methionine cleavage caused by loss of Map1p activity. To better understand the observed fitness defects due to the lack of NMC1 under zinc deficiency, we used proteomics with Tandem Mass Tag (TMT) quantitation derived from WT, nmc1Delta, and map2Delta nmc1Delta strains grown in zinc-limited (1 uM) or zinc-replete (100 uM) conditions. Proteomics reveal global impacts due to the loss of NMC1 and Map1p function, including mis-regulation of the Zap1p regulon, and suggests that Nmc1p is required to avoid a compounding effect of Map1p dysfunction on cell survival during zinc deficiency.
| MSV000088135 | MassIVE
Project description:Mycobacterium tuberculosis H37Rv (Mtb) was grown in Sauton's medium with and without added zinc. Cultures were grown for 10 days and RNA was harvested from TRIzol extractions.
2021-04-21 | GSE168513 | GEO
Project description:Mycobacterium tuberculosis H37Rv (Mtb) grown in chemically defined medium replete for Zinc and limited for Zinc
2021-04-23 | PXD024389 | Pride