ORCID Profile
0000-0001-6015-6806
Current Organisations
National Institutes of Health
,
Tel-Aviv University George S Wise Faculty of Life Sciences
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Publisher: Rockefeller University Press
Date: 29-11-2010
Abstract: PINK1 is a mitochondrial kinase mutated in some familial cases of Parkinson’s disease. It has been found to work in the same pathway as the E3 ligase Parkin in the maintenance of flight muscles and dopaminergic neurons in Drosophila melanogaster and to recruit cytosolic Parkin to mitochondria to mediate mitophagy in mammalian cells. Although PINK1 has a predicted mitochondrial import sequence, its cellular and submitochondrial localization remains unclear in part because it is rapidly degraded. In this study, we report that the mitochondrial inner membrane rhomboid protease presenilin-associated rhomboid-like protein (PARL) mediates cleavage of PINK1 dependent on mitochondrial membrane potential. In the absence of PARL, the constitutive degradation of PINK1 is inhibited, stabilizing a 60-kD form inside mitochondria. When mitochondrial membrane potential is dissipated, PINK1 accumulates as a 63-kD full-length form on the outer mitochondrial membrane, where it can recruit Parkin to impaired mitochondria. Thus, differential localization to the inner and outer mitochondrial membranes appears to regulate PINK1 stability and function.
Publisher: Rockefeller University Press
Date: 17-11-2020
Abstract: Following the detection of cytosolic double-stranded DNA from viral or bacterial infection in mammalian cells, cyclic dinucleotide activation of STING induces interferon β expression to initiate innate immune defenses. STING activation also induces LC3B lipidation, a classical but equivocal marker of autophagy, that promotes a cell-autonomous antiviral response that arose before evolution of the interferon pathway. We report that STING activation induces LC3B lipidation onto single-membrane perinuclear vesicles mediated by ATG16L1 via its WD40 domain, bypassing the requirement of canonical upstream autophagy machinery. This process is blocked by bafilomycin A1 that binds and inhibits the vacuolar ATPase (V-ATPase) and by SopF, a bacterial effector that catalytically modifies the V-ATPase to inhibit LC3B lipidation via ATG16L1. These results indicate that activation of the cGAS-STING pathway induces V-ATPase–dependent LC3B lipidation that may mediate cell-autonomous host defense, an unanticipated mechanism that is distinct from LC3B lipidation onto double-membrane autophagosomes.
Publisher: Wiley
Date: 24-08-2021
DOI: 10.1111/PPA.13450
Abstract: Variation among Puccinia triticina isolates collected from triticale in Poland between 2012 and 2015 was studied based on virulence and simple sequence repeat (SSR) markers. Two hundred and forty‐two single‐uredinial isolates from four geographically separated locations were tested for virulence against 33 near‐isogenic Thatcher lines containing known Lr resistance genes, and their molecular genotypes were characterized with 34 SSR markers. Structure and relationships of the regional and annual populations of P . triticina were analysed using an assignment‐based approach for both the virulence and SSR data. The molecular marker analysis was based on two different models of SSR evolution: the stepwise mutation model with a variable mutation rate (SMMv) and the infinite alleles model (IAM). A highly significant deviation from Hardy–Weinberg equilibrium among SSR genotypes, a high proportion of heterozygotes, and a moderate association of relationships between virulence phenotypes and SSR genotypes were consistent with the occurrence of clonal lineages of related races within the population. While the results suggest that genetic drift and mutation affect variation within the pathogen population, it seems that migration has the most significant role in shaping the population structure of P . triticina occurring on triticale in Poland.
Publisher: Wiley
Date: 10-02-2021
DOI: 10.1111/PPA.13347
Abstract: The aim of the present study was to validate new simple‐sequence repeat (SSR) markers and use them to assess genetic variability among 24 isolates of Puccinia triticina collected from wheat (Pt‐wheat) and triticale (Pt‐triticale), and 15 isolates of P . recondita f. sp. secalis (Prs) collected from rye. The Pt and Prs isolates were tested for virulence on a set of 35 Thatcher wheat near‐isogenic lines, eight rye lines with known resistance genes, and 53 triticale cultivars with uncharacterized leaf rust resistance. Molecular genotypes were determined using a newly developed set of 34 SSR microsatellite primer pairs. All SSR markers tested on Pt isolates successfully lified fragments of appropriate size. When tested on the Prs isolates, 21 out of the 34 Pt SSRs lified expected fragments. Sixteen of these 21 SSRs were polymorphic, providing for the first time microsatellite markers to study genetic variation in Prs. Based on virulence data, variation among Prs isolates was low, probably due to the small number of rye differential lines available. Much higher variation for virulence was observed within the collection of Pt isolates from wheat and triticale, and two separate groups were established with mixed host origin. Substantial genetic variation was detected among the isolates studied with the SSR markers, assuming two different models of SSR evolution (infinite alleles model and stepwise mutation model). The newly developed set of SSR markers proved their effectiveness in detecting genetic variation and should be useful in further population genetics investigations of the two pathogens.
Publisher: Springer Science and Business Media LLC
Date: 08-2015
DOI: 10.1038/NATURE14893
Location: Israel
Location: United States of America
No related grants have been discovered for Chunxin Wang.