Pexophagy is critical for fungal development, stress response, and virulence in Alternaria alternata
Alternaria alternata can resist high levels of reactive oxygen species (ROS). The protective roles of autophagy or autophagy‐mediated degradation of peroxisomes (termed pexophagy) against oxidative stress remain unclear. The present study, using transmission electron microscopy and fluorescence micr...
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| Veröffentlicht in: | Molecular plant pathology 2022-10, Vol.23 (10), p.1538-1554 |
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| creator | Wu, Pei‐Ching Choo, Celine Yen Ling Lu, Hsin‐Yu Wei, Xian‐Yong Chen, Yu‐Kun Yago, Jonar I. Chung, Kuang‐Ren |
| description | Alternaria alternata can resist high levels of reactive oxygen species (ROS). The protective roles of autophagy or autophagy‐mediated degradation of peroxisomes (termed pexophagy) against oxidative stress remain unclear. The present study, using transmission electron microscopy and fluorescence microscopy coupled with a GFP‐AaAtg8 proteolysis assay and an mCherry tagging assay with peroxisomal targeting tripeptides, demonstrated that hydrogen peroxide (H2O2) and nitrogen depletion induced autophagy and pexophagy. Experimental evidence showed that H2O2 triggered autophagy and the translocation of peroxisomes into the vacuoles. Mutational inactivation of the AaAtg8 gene in A. alternata led to autophagy impairment, resulting in the accumulation of peroxisomes, increased ROS sensitivity, and decreased virulence. Compared to the wild type, ΔAaAtg8 failed to detoxify ROS effectively, leading to ROS accumulation. Deleting AaAtg8 down‐regulated the expression of genes encoding an NADPH oxidase and a Yap1 transcription factor, both involved in ROS resistance. Deleting AaAtg8 affected the development of conidia and appressorium‐like structures. Deleting AaAtg8 also compromised the integrity of the cell wall. Reintroduction of a functional copy of AaAtg8 in the mutant completely restored all defective phenotypes. Although ΔAaAtg8 produced wild‐type toxin levels in axenic culture, the mutant induced a lower level of H2O2 and smaller necrotic lesions on citrus leaves. In addition to H2O2, nitrogen starvation triggered peroxisome turnover. We concluded that ΔAaAtg8 failed to degrade peroxisomes effectively, leading to the accumulation of peroxisomes and the reduction of the stress response. Autophagy‐mediated peroxisome turnover could increase cell adaptability and survival under oxidative stress and starvation conditions.
The degradation of peroxisomes, resistance to oxidative stress, nutrient recycling, and pathogenicity is mediated by pexophagy in Alternaria alternata. |
| doi_str_mv | 10.1111/mpp.13247 |
| format | Article |
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The degradation of peroxisomes, resistance to oxidative stress, nutrient recycling, and pathogenicity is mediated by pexophagy in Alternaria alternata.</description><identifier>ISSN: 1464-6722</identifier><identifier>EISSN: 1364-3703</identifier><identifier>DOI: 10.1111/mpp.13247</identifier><identifier>PMID: 35810316</identifier><language>eng</language><publisher>Oxford: John Wiley & Sons, Inc</publisher><subject>Accumulation ; Adaptability ; Alternaria alternata ; Amino acids ; Apoptosis ; Atg8 ; Autophagy ; Cell culture ; Cell survival ; Cell walls ; Conidia ; Depletion ; Fluorescence ; Fluorescence microscopy ; Fungi ; Gene expression ; Germfree ; Homeostasis ; Hydrogen peroxide ; Inactivation ; Lipids ; Metabolism ; Microscopy ; Mutants ; NAD(P)H oxidase ; Nitrogen ; Original ; Oxidative stress ; peroxisome ; Peroxisomes ; Pexophagy ; Phenotypes ; Protected species ; Proteins ; Proteolysis ; Pure culture ; Reactive oxygen species ; Reintroduction ; ROS detoxification ; Starvation ; stress tolerance ; Toxins ; Translocation ; Transmission electron microscopy ; Vacuoles ; Virulence</subject><ispartof>Molecular plant pathology, 2022-10, Vol.23 (10), p.1538-1554</ispartof><rights>2022 The Authors. published by British Society for Plant Pathology and John Wiley & Sons Ltd.</rights><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3897-7b836ae30e1fb4e5042b82aad02620e7ecce2dc7f319d81d3ca9d2968d8a04523</citedby><cites>FETCH-LOGICAL-c3897-7b836ae30e1fb4e5042b82aad02620e7ecce2dc7f319d81d3ca9d2968d8a04523</cites><orcidid>0000-0002-2640-2951 ; 0000-0001-7678-2078</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9452759/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9452759/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids></links><search><creatorcontrib>Wu, Pei‐Ching</creatorcontrib><creatorcontrib>Choo, Celine Yen Ling</creatorcontrib><creatorcontrib>Lu, Hsin‐Yu</creatorcontrib><creatorcontrib>Wei, Xian‐Yong</creatorcontrib><creatorcontrib>Chen, Yu‐Kun</creatorcontrib><creatorcontrib>Yago, Jonar I.</creatorcontrib><creatorcontrib>Chung, Kuang‐Ren</creatorcontrib><title>Pexophagy is critical for fungal development, stress response, and virulence in Alternaria alternata</title><title>Molecular plant pathology</title><description>Alternaria alternata can resist high levels of reactive oxygen species (ROS). The protective roles of autophagy or autophagy‐mediated degradation of peroxisomes (termed pexophagy) against oxidative stress remain unclear. The present study, using transmission electron microscopy and fluorescence microscopy coupled with a GFP‐AaAtg8 proteolysis assay and an mCherry tagging assay with peroxisomal targeting tripeptides, demonstrated that hydrogen peroxide (H2O2) and nitrogen depletion induced autophagy and pexophagy. Experimental evidence showed that H2O2 triggered autophagy and the translocation of peroxisomes into the vacuoles. Mutational inactivation of the AaAtg8 gene in A. alternata led to autophagy impairment, resulting in the accumulation of peroxisomes, increased ROS sensitivity, and decreased virulence. Compared to the wild type, ΔAaAtg8 failed to detoxify ROS effectively, leading to ROS accumulation. Deleting AaAtg8 down‐regulated the expression of genes encoding an NADPH oxidase and a Yap1 transcription factor, both involved in ROS resistance. Deleting AaAtg8 affected the development of conidia and appressorium‐like structures. Deleting AaAtg8 also compromised the integrity of the cell wall. Reintroduction of a functional copy of AaAtg8 in the mutant completely restored all defective phenotypes. Although ΔAaAtg8 produced wild‐type toxin levels in axenic culture, the mutant induced a lower level of H2O2 and smaller necrotic lesions on citrus leaves. In addition to H2O2, nitrogen starvation triggered peroxisome turnover. We concluded that ΔAaAtg8 failed to degrade peroxisomes effectively, leading to the accumulation of peroxisomes and the reduction of the stress response. Autophagy‐mediated peroxisome turnover could increase cell adaptability and survival under oxidative stress and starvation conditions.
The degradation of peroxisomes, resistance to oxidative stress, nutrient recycling, and pathogenicity is mediated by pexophagy in Alternaria alternata.</description><subject>Accumulation</subject><subject>Adaptability</subject><subject>Alternaria alternata</subject><subject>Amino acids</subject><subject>Apoptosis</subject><subject>Atg8</subject><subject>Autophagy</subject><subject>Cell culture</subject><subject>Cell survival</subject><subject>Cell walls</subject><subject>Conidia</subject><subject>Depletion</subject><subject>Fluorescence</subject><subject>Fluorescence microscopy</subject><subject>Fungi</subject><subject>Gene expression</subject><subject>Germfree</subject><subject>Homeostasis</subject><subject>Hydrogen peroxide</subject><subject>Inactivation</subject><subject>Lipids</subject><subject>Metabolism</subject><subject>Microscopy</subject><subject>Mutants</subject><subject>NAD(P)H oxidase</subject><subject>Nitrogen</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>peroxisome</subject><subject>Peroxisomes</subject><subject>Pexophagy</subject><subject>Phenotypes</subject><subject>Protected species</subject><subject>Proteins</subject><subject>Proteolysis</subject><subject>Pure culture</subject><subject>Reactive oxygen species</subject><subject>Reintroduction</subject><subject>ROS detoxification</subject><subject>Starvation</subject><subject>stress tolerance</subject><subject>Toxins</subject><subject>Translocation</subject><subject>Transmission electron microscopy</subject><subject>Vacuoles</subject><subject>Virulence</subject><issn>1464-6722</issn><issn>1364-3703</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1UU1r3DAUFKWh-WgP_QeCngrZjb5s2ZfCEtq0kNA9tGehlZ43CrbkSvYm--_7UodCD5VAb5Bmhqc3hLznbM1xXQ3juOZSKP2KnHFZq5XUTL5GrBDXWohTcl7KA2Nct6J6Q05l1XAmeX1G_Bae0nhv90caCnU5TMHZnnYp026Oe4QeDtCncYA4XdIyZSiF4jGmWOCS2ujpIeS5h-iAhkg3_QQ52hwstQuc7Fty0tm-wLuXekF-fvn84_rr6vb7zbfrze3KyabVK71rZG1BMuDdTkHFlNg1wlrPRC0YaHAOhHe6k7z1DffS2daLtm58Y5mqhLwgnxbfcd4N4B22nG1vxhwGm48m2WD-fYnh3uzTwbSo1lWLBh9eDHL6NUOZzEOa8Qt9MULjpJmUSiFrvbBwPGBC7BKaOdwehuBShC7g_UYrrpismUbBx0XgciolQ_e3Jc7Mc4IGEzR_EkTu1cJ9RJPj_4nmbrtdFL8BAbSddw</recordid><startdate>202210</startdate><enddate>202210</enddate><creator>Wu, Pei‐Ching</creator><creator>Choo, Celine Yen Ling</creator><creator>Lu, Hsin‐Yu</creator><creator>Wei, Xian‐Yong</creator><creator>Chen, Yu‐Kun</creator><creator>Yago, Jonar I.</creator><creator>Chung, Kuang‐Ren</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons 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alternata</title><author>Wu, Pei‐Ching ; Choo, Celine Yen Ling ; Lu, Hsin‐Yu ; Wei, Xian‐Yong ; Chen, Yu‐Kun ; Yago, Jonar I. ; Chung, Kuang‐Ren</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3897-7b836ae30e1fb4e5042b82aad02620e7ecce2dc7f319d81d3ca9d2968d8a04523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Accumulation</topic><topic>Adaptability</topic><topic>Alternaria alternata</topic><topic>Amino acids</topic><topic>Apoptosis</topic><topic>Atg8</topic><topic>Autophagy</topic><topic>Cell culture</topic><topic>Cell survival</topic><topic>Cell walls</topic><topic>Conidia</topic><topic>Depletion</topic><topic>Fluorescence</topic><topic>Fluorescence microscopy</topic><topic>Fungi</topic><topic>Gene expression</topic><topic>Germfree</topic><topic>Homeostasis</topic><topic>Hydrogen peroxide</topic><topic>Inactivation</topic><topic>Lipids</topic><topic>Metabolism</topic><topic>Microscopy</topic><topic>Mutants</topic><topic>NAD(P)H oxidase</topic><topic>Nitrogen</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>peroxisome</topic><topic>Peroxisomes</topic><topic>Pexophagy</topic><topic>Phenotypes</topic><topic>Protected species</topic><topic>Proteins</topic><topic>Proteolysis</topic><topic>Pure culture</topic><topic>Reactive oxygen species</topic><topic>Reintroduction</topic><topic>ROS detoxification</topic><topic>Starvation</topic><topic>stress tolerance</topic><topic>Toxins</topic><topic>Translocation</topic><topic>Transmission electron microscopy</topic><topic>Vacuoles</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Pei‐Ching</creatorcontrib><creatorcontrib>Choo, Celine Yen Ling</creatorcontrib><creatorcontrib>Lu, Hsin‐Yu</creatorcontrib><creatorcontrib>Wei, 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pathology</jtitle><date>2022-10</date><risdate>2022</risdate><volume>23</volume><issue>10</issue><spage>1538</spage><epage>1554</epage><pages>1538-1554</pages><issn>1464-6722</issn><eissn>1364-3703</eissn><abstract>Alternaria alternata can resist high levels of reactive oxygen species (ROS). The protective roles of autophagy or autophagy‐mediated degradation of peroxisomes (termed pexophagy) against oxidative stress remain unclear. The present study, using transmission electron microscopy and fluorescence microscopy coupled with a GFP‐AaAtg8 proteolysis assay and an mCherry tagging assay with peroxisomal targeting tripeptides, demonstrated that hydrogen peroxide (H2O2) and nitrogen depletion induced autophagy and pexophagy. Experimental evidence showed that H2O2 triggered autophagy and the translocation of peroxisomes into the vacuoles. Mutational inactivation of the AaAtg8 gene in A. alternata led to autophagy impairment, resulting in the accumulation of peroxisomes, increased ROS sensitivity, and decreased virulence. Compared to the wild type, ΔAaAtg8 failed to detoxify ROS effectively, leading to ROS accumulation. Deleting AaAtg8 down‐regulated the expression of genes encoding an NADPH oxidase and a Yap1 transcription factor, both involved in ROS resistance. Deleting AaAtg8 affected the development of conidia and appressorium‐like structures. Deleting AaAtg8 also compromised the integrity of the cell wall. Reintroduction of a functional copy of AaAtg8 in the mutant completely restored all defective phenotypes. Although ΔAaAtg8 produced wild‐type toxin levels in axenic culture, the mutant induced a lower level of H2O2 and smaller necrotic lesions on citrus leaves. In addition to H2O2, nitrogen starvation triggered peroxisome turnover. We concluded that ΔAaAtg8 failed to degrade peroxisomes effectively, leading to the accumulation of peroxisomes and the reduction of the stress response. Autophagy‐mediated peroxisome turnover could increase cell adaptability and survival under oxidative stress and starvation conditions.
The degradation of peroxisomes, resistance to oxidative stress, nutrient recycling, and pathogenicity is mediated by pexophagy in Alternaria alternata.</abstract><cop>Oxford</cop><pub>John Wiley & Sons, Inc</pub><pmid>35810316</pmid><doi>10.1111/mpp.13247</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-2640-2951</orcidid><orcidid>https://orcid.org/0000-0001-7678-2078</orcidid><oa>free_for_read</oa></addata></record> |
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| source | DOAJ Directory of Open Access Journals; Access via Wiley Online Library; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Accumulation Adaptability Alternaria alternata Amino acids Apoptosis Atg8 Autophagy Cell culture Cell survival Cell walls Conidia Depletion Fluorescence Fluorescence microscopy Fungi Gene expression Germfree Homeostasis Hydrogen peroxide Inactivation Lipids Metabolism Microscopy Mutants NAD(P)H oxidase Nitrogen Original Oxidative stress peroxisome Peroxisomes Pexophagy Phenotypes Protected species Proteins Proteolysis Pure culture Reactive oxygen species Reintroduction ROS detoxification Starvation stress tolerance Toxins Translocation Transmission electron microscopy Vacuoles Virulence |
| title | Pexophagy is critical for fungal development, stress response, and virulence in Alternaria alternata |
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