ArticlePLoS pathogens2019
The selective autophagy receptors Optineurin and p62 are both required for zebrafish host resistance to mycobacterial infection.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Microglia maintain retinal redox homeostasis following ablation of rod photoreceptors in zebrafish.The Journal of biological chemistry · 2026Article
- Recommendations of the Polish Zebrafish Society on the use of the zebrafish (Acta biochimica Polonica · 2026Review
- PIKfyve mediates the maturation of mycobacteria-containing vesicles.Frontiers in cellular and infection microbiology · 2026Article
- Pneumolysin-dependent and independent non-canonical autophagy processes mediate host defense against pneumococcal infection.Autophagy · 2025Article
- Loss of the Ubiquitin-Associated Domain of sqstm1/p62 in Zebrafish Causes a Phenotype Resembling Paget's Disease of Bone.Calcified tissue international · 2025Article
- An mRNA vaccine induces antimycobacterial immunity by activating DNA damage repair and autophagy.Molecular therapy. Nucleic acids · 2025Article
- LRSAM1 mediated the degradation of intracellular Vibrio through the ubiquitination-autophagy-lysosome pathway in oyster.Cell communication and signaling : CCS · 2025Article
- Review
- Autophagy in mycobacterial infections: molecular mechanisms, host-pathogen interactions, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Lessons from cross-pathogen studies: understanding the metabolic rewiring of macrophages upon infection.Frontiers in cellular and infection microbiology · 2025Review
- A cytoprotective role for optineurin during mycobacterial infection of macrophages.Biochemistry and biophysics reports · 2024Article
- Establishment of a zebrafish inbred strain, M-AB, capable of regular breeding and genetic manipulation.Scientific reports · 2024Article
- Seneca Valley virus 3C protease cleaves OPTN (optineurin) to Impair selective autophagy and type I interferon signaling.Autophagy · 2024Article
- TLR-mediated aggresome-like induced structures comprise antimicrobial peptides and attenuate intracellular bacterial survival.Molecular biology of the cell · 2024Article
- TRAF6 triggers Mycobacterium-infected host autophagy through Rab7 ubiquitination.Cell death discovery · 2023Article
- The Interplay of Genital Herpes with Cellular Processes: A Pathogenesis and Therapeutic Perspective.Viruses · 2023Review
- Using Zebrafish to Dissect the Interaction of Mycobacteria with the Autophagic Machinery in Macrophages.Biology · 2023Article
- Article
- Enhanced liquidity of p62 droplets mediated by Smurf1 links Nrf2 activation and autophagy.Cell & bioscience · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterial pathogens are the causative agents of chronic infectious diseases like tuberculosis and leprosy. Autophagy has recently emerged as an innate mechanism for defense against these intracellular pathogens. In vitro studies have shown that mycobacteria escaping from phagosomes into the cytosol are ubiquitinated and targeted by selective autophagy receptors. However, there is currently no in vivo evidence for the role of selective autophagy receptors in defense against mycobacteria, and the importance of autophagy in control of mycobacterial diseases remains controversial. Here we have used Mycobacterium marinum (Mm), which causes a tuberculosis-like disease in zebrafish, to investigate the function of two selective autophagy receptors, Optineurin (Optn) and SQSTM1 (p62), in host defense against a mycobacterial pathogen. To visualize the autophagy response to Mm in vivo, optn and p62 zebrafish mutant lines were generated in the background of a GFP-Lc3 autophagy reporter line. We found that loss-of-function mutation of optn or p62 reduces autophagic targeting of Mm, and increases susceptibility of the zebrafish host to Mm infection. Transient knockdown studies confirmed the requirement of both selective autophagy receptors for host resistance against Mm infection. For gain-of-function analysis, we overexpressed optn or p62 by mRNA injection and found this to increase the levels of GFP-Lc3 puncta in association with Mm and to reduce the Mm infection burden. Taken together, our results demonstrate that both Optn and p62 are required for autophagic host defense against mycobacterial infection and support that protection against tuberculosis disease may be achieved by therapeutic strategies that enhance selective autophagy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.