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A Survey of Serine Hydrolase Activity in Mycobacterium tuberculosis

ABSTRACT: Changes in Serine Hydrolase Activity Associated with Mycobacterium tuberculosis Replication

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Mycobacterium Tuberculosis

TISSUE(S): Blood Cell, Blood

DISEASE(S): Breast Cancer

SUBMITTER: Matthew Monroe

LAB HEAD: Aaron T. Wright

PROVIDER: PXD002763 | Pride | 2016-02-01

REPOSITORIES: Pride

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			Action	DRS
	Mtb_NP_A_7Jul14_Lynx_14-02-24.mgf	Mgf
	Mtb_NP_A_7Jul14_Lynx_14-02-24.pride.mgf.gz	Mgf
	Mtb_NP_A_7Jul14_Lynx_14-02-24.raw	Raw
	Mtb_NP_A_7Jul14_Lynx_14-02-24_msgfplus.mzid.gz	Mzid
	Mtb_NP_A_7Jul14_Lynx_14-02-24_msgfplus.pride.mztab.gz	Mztab

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Publications

Systematic Survey of Serine Hydrolase Activity in Mycobacterium tuberculosis Defines Changes Associated with Persistence.

Ortega Corrie C Anderson Lindsey N LN Frando Andrew A Sadler Natalie C NC Brown Robert W RW Smith Richard D RD Wright Aaron T AT Grundner Christoph C

Cell chemical biology 20160204 2

The transition from replication to non-replication underlies much of Mycobacterium tuberculosis (Mtb) pathogenesis, as non- or slowly replicating Mtb are responsible for persistence and poor treatment outcomes. Therapeutic targeting of non-replicating populations is a priority for tuberculosis treatment, but few drug targets in non-replicating Mtb are currently known. Here, we directly measured the activity of the highly diverse and druggable serine hydrolases (SHs) during active replication and ...[more]

PMID: 26853625

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Systematic Survey of Serine Hydrolase Activity in Mycobacterium tuberculosis Defines Changes Associated with Persistence.

Project description:The transition from replication to non-replication underlies much of Mycobacterium tuberculosis (Mtb) pathogenesis, as non- or slowly replicating Mtb are responsible for persistence and poor treatment outcomes. Therapeutic targeting of non-replicating populations is a priority for tuberculosis treatment, but few drug targets in non-replicating Mtb are currently known. Here, we directly measured the activity of the highly diverse and druggable serine hydrolases (SHs) during active replication and non-replication using activity-based proteomics. We predict SH activity for 78 proteins, including 27 proteins with unknown function, and identify 37 SHs that remain active in the absence of replication, providing a set of candidate persistence targets. Non-replication was associated with major shifts in SH activity. These activity changes were largely independent of SH abundance, indicating extensive post-translational regulation of SHs. By probing a large cross-section of druggable Mtb enzyme space during replication and non-replication, we identify new SHs and suggest new persistence targets.

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Mycobacterium tuberculosis impairs dendritic cell functions through the serine hydrolase Hip1.

Project description:Mycobacterium tuberculosis is a highly successful human pathogen that primarily resides in host phagocytes, such as macrophages and dendritic cells (DCs), and interferes with their functions. Although multiple strategies used by M. tuberculosis to modulate macrophage responses have been discovered, interactions between M. tuberculosis and DCs are less well understood. DCs are the primary APCs of the immune system and play a central role in linking innate and adaptive immune responses to microbial pathogens. In this study, we show that M. tuberculosis impairs DC cytokine secretion, maturation, and Ag presentation through the cell envelope-associated serine hydrolase, Hip1. Compared to wild-type, a hip1 mutant strain of M. tuberculosis induced enhanced levels of the key Th1-inducing cytokine IL-12, as well as other proinflammatory cytokines (IL-23, IL-6, TNF-?, IL-1?, and IL-18) in DCs via MyD88- and TLR2/9-dependent pathways, indicating that Hip1 restricts optimal DC inflammatory responses. Infection with the hip1 mutant also induced higher levels of MHC class II and costimulatory molecules CD40 and CD86, indicating that M. tuberculosis impairs DC maturation through Hip1. Further, we show that M. tuberculosis promotes suboptimal Ag presentation, as DCs infected with the hip1 mutant showed increased capacity to present Ag to OT-II- and early secreted antigenic target 6-specific transgenic CD4 T cells and enhanced Th1 and Th17 polarization. Overall, these data show that M. tuberculosis impairs DC functions and modulates the nature of Ag-specific T cell responses, with important implications for vaccination strategies.

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