Dataset Information

Proteomics of Zinc-limited Mycobacterium tuberculosis

ABSTRACT: Mycobacterium tuberculosis H37Rv (Mtb) grown in chemically defined medium replete for Zinc and limited for Zinc

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mycobacterium Tuberculosis H37rv

SUBMITTER: Endrei Marcantonio

LAB HEAD: Sladjana Prisic

PROVIDER: PXD024389 | Pride | 2021-04-23

REPOSITORIES: Pride

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Publications

Zinc limitation triggers anticipatory adaptations in Mycobacterium tuberculosis.

Dow Allexa A Sule Preeti P O'Donnell Timothy J TJ Burger Andrew A Mattila Joshua T JT Antonio Brandi B Vergara Kevin K Marcantonio Endrei E Adams L Garry LG James Nicholas N Williams Philip G PG Cirillo Jeffrey D JD Prisic Sladjana S

PLoS pathogens 20210514 5

Mycobacterium tuberculosis (Mtb) has complex and dynamic interactions with the human host, and subpopulations of Mtb that emerge during infection can influence disease outcomes. This study implicates zinc ion (Zn2+) availability as a likely driver of bacterial phenotypic heterogeneity in vivo. Zn2+ sequestration is part of "nutritional immunity", where the immune system limits micronutrients to control pathogen growth, but this defense mechanism seems to be ineffective in controlling Mtb infecti ...[more]

PMID: 33989345

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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 ÂµM Zn-EDTA The control samples for this study are represented in GSE25622

Dataset Information

Proteomics of Zinc-limited Mycobacterium tuberculosis

Publications

Zinc limitation triggers anticipatory adaptations in Mycobacterium tuberculosis.

Similar Datasets

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