Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 401533
Title ClgR regulation of chaperone and protease systems is essential for Mycobacterium tuberculosis parasitism of the macrophage
Author(s) Estorninho, M.; Smith, H.E.; Thole, J.E.R.; Harders-Westerveen, S.F.; Kierzek, A.; Butler, R.E.; Neyrolles, O.; Stewart, G.R.
Source Microbiology 156 (2010). - ISSN 1350-0872 - p. 3445 - 3455.
Department(s) CVI Infection Biology
ASG Infectieziekten
Publication type Refereed Article in a scientific journal
Publication year 2010
Keyword(s) gram-positive bacteria - sigma-factor sigma(h) - heat-shock response - alpha-crystallin - corynebacterium-glutamicum - bacillus-subtilis - gene-expression - microarray data - quality-control - clp atpases
Abstract Chaperone and protease systems play essential roles in cellular homeostasis and have vital functions in controlling the abundance of specific cellular proteins involved in processes such as transcription, replication, metabolism and virulence. Bacteria have evolved accurate regulatory systems to control the expression and function of chaperones and potentially destructive proteases. Here, we have used a combination of transcriptomics, proteomics and targeted mutagenesis to reveal that the clp gene regulator (ClgR) of Mycobacterium tuberculosis activates the transcription of at least ten genes, including four that encode protease systems (ClpP1/C, ClpP2/C, PtrB and HtrA-like protease Rv1043c) and three that encode chaperones (Acr2, ClpB and the chaperonin Rv3269). Thus, M. tuberculosis ClgR controls a larger network of protein homeostatic and regulatory systems than ClgR in any other bacterium studied to date. We demonstrate that ClgR-regulated transcriptional activation of these systems is essential for M. tuberculosis to replicate in macrophages. Furthermore, we observe that this defect is manifest early in infection, as M. tuberculosis lacking ClgR is deficient in the ability to control phagosome pH 1 h post-phagocytosis.
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