Potential role of autophagy in proteolysis in Trichomonas vaginalis.


Journal

Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi
ISSN: 1995-9133
Titre abrégé: J Microbiol Immunol Infect
Pays: England
ID NLM: 100956211

Informations de publication

Date de publication:
Apr 2019
Historique:
received: 14 08 2018
revised: 09 10 2018
accepted: 16 11 2018
pubmed: 7 12 2018
medline: 30 4 2019
entrez: 4 12 2018
Statut: ppublish

Résumé

Autophagy has been shown to be involved in the pathogenesis of several protists, offering prospects for the developments of new drugs targeting autophagy. However, there is no evidence illustrating functional autophagy in the deep-branching trichomonads. The human parasitic protist Trichomonas vaginalis has been predicted to possess reduced autophagic machinery, with only autophagy-related protein 8 (Atg8) conjugation system required for autophagosome formation. The recombinant protein of TvAtg8 (rTvAtg8) and the polyclonal antibody against rTvAtg8 were generated. The expression and localization of TvAtg8 was monitored upon autophagy induction by glucose restriction (GR) compared with glucose-rich cultivation. The role of TvAtg8 in proteolysis was clarified. Here, we report that T. vaginalis Atg8 (TvAtg8) is upregulated and conjugated to autophagosome-like vesicles upon autophagy induction by GR. Moreover, we investigate, for the first time, the role of autophagy in T. vaginalis. Proteasome inhibition (PI)-induced autophagy compensates for the removal of polyubiquitinated proteins under glucose-rich condition. GR-induced autophagy is a major proteolytic system in T. vaginalis. These results suggest that autophagy is vital for proteolysis in T. vaginalis with an impaired ubiquitin-proteasome system or under glucose-limited environment. Our findings unveiled previously unidentified functions of autophagy in proteostasis in trichomonads, advancing our understanding of this highly conserved process in the ancient eukaryote.

Sections du résumé

BACKGROUND BACKGROUND
Autophagy has been shown to be involved in the pathogenesis of several protists, offering prospects for the developments of new drugs targeting autophagy. However, there is no evidence illustrating functional autophagy in the deep-branching trichomonads. The human parasitic protist Trichomonas vaginalis has been predicted to possess reduced autophagic machinery, with only autophagy-related protein 8 (Atg8) conjugation system required for autophagosome formation.
METHODS METHODS
The recombinant protein of TvAtg8 (rTvAtg8) and the polyclonal antibody against rTvAtg8 were generated. The expression and localization of TvAtg8 was monitored upon autophagy induction by glucose restriction (GR) compared with glucose-rich cultivation. The role of TvAtg8 in proteolysis was clarified.
RESULTS RESULTS
Here, we report that T. vaginalis Atg8 (TvAtg8) is upregulated and conjugated to autophagosome-like vesicles upon autophagy induction by GR. Moreover, we investigate, for the first time, the role of autophagy in T. vaginalis. Proteasome inhibition (PI)-induced autophagy compensates for the removal of polyubiquitinated proteins under glucose-rich condition. GR-induced autophagy is a major proteolytic system in T. vaginalis. These results suggest that autophagy is vital for proteolysis in T. vaginalis with an impaired ubiquitin-proteasome system or under glucose-limited environment.
CONCLUSION CONCLUSIONS
Our findings unveiled previously unidentified functions of autophagy in proteostasis in trichomonads, advancing our understanding of this highly conserved process in the ancient eukaryote.

Identifiants

pubmed: 30503389
pii: S1684-1182(18)30301-3
doi: 10.1016/j.jmii.2018.11.002
pii:
doi:

Substances chimiques

Autophagy-Related Protein 8 Family 0
Leupeptins 0
Proteasome Inhibitors 0
Recombinant Proteins 0
Proteasome Endopeptidase Complex EC 3.4.25.1
Glucose IY9XDZ35W2
benzyloxycarbonylleucyl-leucyl-leucine aldehyde RF1P63GW3K

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

336-344

Informations de copyright

Copyright © 2018. Published by Elsevier B.V.

Auteurs

Kuo-Yang Huang (KY)

Graduate Institute of Pathology and Parasitology, National Defense Medical Center, Taipei City, Taiwan.

Ruei-Min Chen (RM)

Division of Clinical Pathology, Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei City, Taiwan.

Hsin-Chung Lin (HC)

Division of Clinical Pathology, Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei City, Taiwan; Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei City, Taiwan.

Wei-Hung Cheng (WH)

Molecular Regulation and Bioinformatics Laboratory, Department of Parasitology, College of Medicine, Chang Gung University, Taoyuan City, Taiwan.

Hsin-An Lin (HA)

Division of Infection, Department of Medicine, Tri-Service General Hospital SongShan Branch, Taipei City, Taiwan.

Wei-Ning Lin (WN)

Graduate Institute of Biomedical and Pharmaceutical Science, Fu Jen Catholic University, New Taipei City, Taiwan.

Po-Jung Huang (PJ)

Department of Biomedical Sciences, Chang Gung University, Taoyuan City, Taiwan; Genomic Medicine Core Laboratory, Chang Gung Memorial Hospital, Linkou, Taiwan.

Cheng-Hsun Chiu (CH)

Molecular Infectious Diseases Research Center, Chang Gung Memorial Hospital, Taoyuan City, Taiwan.

Petrus Tang (P)

Molecular Regulation and Bioinformatics Laboratory, Department of Parasitology, College of Medicine, Chang Gung University, Taoyuan City, Taiwan; Molecular Infectious Diseases Research Center, Chang Gung Memorial Hospital, Taoyuan City, Taiwan. Electronic address: petang@mail.cgu.edu.tw.

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Classifications MeSH