Journal
JOURNAL OF BACTERIOLOGY
Volume 194, Issue 4, Pages 884-893Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.06417-11
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Funding
- Canadian Thoracic Society
- Canadian Institutes of Health Research
- European Community [201762]
- Swiss National Science Foundation [31003A-125061]
- National Institutes of Health, National Institute of Allergy and Infectious Diseases [HHSN266200400091c]
- Swiss National Science Foundation (SNF) [31003A_125061] Funding Source: Swiss National Science Foundation (SNF)
- Medical Research Council [MC_U117585867] Funding Source: researchfish
- MRC [MC_U117585867] Funding Source: UKRI
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ESAT-6 system 1 (ESX-1)-mediated secretion in Mycobacterium tuberculosis is dependent on proteins encoded by the cotranscribed espA-espC-espD gene cluster. While the roles of EspA and EspC with respect to the ESX-1 secretion system have been actively investigated, the function of EspD remains unknown. We show that EspD is secreted by M. tuberculosis, but unlike EspA and EsxA, its export does not exclusively require the ESX-1 system. Evidence for stabilization of cellular levels of EspA and EspC by EspD is presented, and depletion of EspD results in loss of EsxA secretion. Site-directed mutagenesis of EspD reveals that its role in the maintenance of cellular levels of EspA in M. tuberculosis is distinct from its facilitation of EsxA secretion. The same mutagenesis experiments have also shown that secretion of EspD is not required for the secretion of EsxA. Our findings highlight a critical and complex role for EspD in modulating the ESX-1 secretion system in M. tuberculosis.
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