Host Plant Strategies to Combat Against Viruses Effector Proteins.
Identifieur interne : 000141 ( Main/Exploration ); précédent : 000140; suivant : 000142Host Plant Strategies to Combat Against Viruses Effector Proteins.
Auteurs : Avinash Marwal [Inde] ; Rajarshi Kumar Gaur [Inde]Source :
- Current genomics [ 1389-2029 ] ; 2020.
Abstract
Viruses are obligate parasites that exist in an inactive state until they enter the host body. Upon entry, viruses become active and start replicating by using the host cell machinery. All plant viruses can augment their transmission, thus powering their detrimental effects on the host plant. To diminish infection and diseases caused by viruses, the plant has a defence mechanism known as pathogenesis-related biochemicals, which are metabolites and proteins. Proteins that ultimately prevent pathogenic diseases are called R proteins. Several plant R genes (that confirm resistance) and avirulence protein (Avr) (pathogen Avr gene-encoded proteins [effector/elicitor proteins involved in pathogenicity]) molecules have been identified. The recognition of such a factor results in the plant defence mechanism. During plant viral infection, the replication and expression of a viral molecule lead to a series of a hypersensitive response (HR) and affect the host plant's immunity (pathogen-associated molecular pattern-triggered immunity and effector-triggered immunity). Avr protein renders the host RNA silencing mechanism and its innate immunity, chiefly known as silencing suppressors towards the plant defensive machinery. This is a strong reply to the plant defensive machinery by harmful plant viruses. In this review, we describe the plant pathogen resistance protein and how these proteins regulate host immunity during plant-virus interactions. Furthermore, we have discussed regarding ribosome-inactivating proteins, ubiquitin proteasome system, translation repression (nuclear shuttle protein interacting kinase 1), DNA methylation, dominant resistance genes, and autophagy-mediated protein degradation, which are crucial in antiviral defences.
DOI: 10.2174/1389202921999200712135131
PubMed: 33093803
PubMed Central: PMC7536791
Affiliations:
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Upon entry, viruses become active and start replicating by using the host cell machinery. All plant viruses can augment their transmission, thus powering their detrimental effects on the host plant. To diminish infection and diseases caused by viruses, the plant has a defence mechanism known as pathogenesis-related biochemicals, which are metabolites and proteins. Proteins that ultimately prevent pathogenic diseases are called R proteins. Several plant R genes (that confirm resistance) and avirulence protein (Avr) (pathogen Avr gene-encoded proteins [effector/elicitor proteins involved in pathogenicity]) molecules have been identified. The recognition of such a factor results in the plant defence mechanism. During plant viral infection, the replication and expression of a viral molecule lead to a series of a hypersensitive response (HR) and affect the host plant's immunity (pathogen-associated molecular pattern-triggered immunity and effector-triggered immunity). Avr protein renders the host RNA silencing mechanism and its innate immunity, chiefly known as silencing suppressors towards the plant defensive machinery. This is a strong reply to the plant defensive machinery by harmful plant viruses. In this review, we describe the plant pathogen resistance protein and how these proteins regulate host immunity during plant-virus interactions. Furthermore, we have discussed regarding ribosome-inactivating proteins, ubiquitin proteasome system, translation repression (nuclear shuttle protein interacting kinase 1), DNA methylation, dominant resistance genes, and autophagy-mediated protein degradation, which are crucial in antiviral defences.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">33093803</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1389-2029</ISSN><JournalIssue CitedMedium="Print"><Volume>21</Volume><Issue>6</Issue><PubDate><Year>2020</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Current genomics</Title><ISOAbbreviation>Curr Genomics</ISOAbbreviation></Journal><ArticleTitle>Host Plant Strategies to Combat Against Viruses Effector Proteins.</ArticleTitle><Pagination><MedlinePgn>401-410</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2174/1389202921999200712135131</ELocationID><Abstract><AbstractText>Viruses are obligate parasites that exist in an inactive state until they enter the host body. Upon entry, viruses become active and start replicating by using the host cell machinery. All plant viruses can augment their transmission, thus powering their detrimental effects on the host plant. To diminish infection and diseases caused by viruses, the plant has a defence mechanism known as pathogenesis-related biochemicals, which are metabolites and proteins. Proteins that ultimately prevent pathogenic diseases are called R proteins. Several plant R genes (that confirm resistance) and avirulence protein (Avr) (pathogen Avr gene-encoded proteins [effector/elicitor proteins involved in pathogenicity]) molecules have been identified. The recognition of such a factor results in the plant defence mechanism. During plant viral infection, the replication and expression of a viral molecule lead to a series of a hypersensitive response (HR) and affect the host plant's immunity (pathogen-associated molecular pattern-triggered immunity and effector-triggered immunity). Avr protein renders the host RNA silencing mechanism and its innate immunity, chiefly known as silencing suppressors towards the plant defensive machinery. This is a strong reply to the plant defensive machinery by harmful plant viruses. In this review, we describe the plant pathogen resistance protein and how these proteins regulate host immunity during plant-virus interactions. Furthermore, we have discussed regarding ribosome-inactivating proteins, ubiquitin proteasome system, translation repression (nuclear shuttle protein interacting kinase 1), DNA methylation, dominant resistance genes, and autophagy-mediated protein degradation, which are crucial in antiviral defences.</AbstractText><CopyrightInformation>© 2020 Bentham Science Publishers.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Marwal</LastName><ForeName>Avinash</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>1Department of Biotechnology, Vigyan Bhawan - Block B, New Campus, Mohanlal Sukhadia University, Udaipur, Rajasthan - 313001, India; 2Department of Biotechnology, Deen Dayal Upadhyay Gorakhpur University, Gorakhpur, Uttar Pradesh - 273009, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gaur</LastName><ForeName>Rajarshi Kumar</ForeName><Initials>RK</Initials><AffiliationInfo><Affiliation>1Department of Biotechnology, Vigyan Bhawan - Block B, New Campus, Mohanlal Sukhadia University, Udaipur, Rajasthan - 313001, India; 2Department of Biotechnology, Deen Dayal Upadhyay Gorakhpur University, Gorakhpur, Uttar Pradesh - 273009, India.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United Arab Emirates</Country><MedlineTA>Curr Genomics</MedlineTA><NlmUniqueID>100960527</NlmUniqueID><ISSNLinking>1389-2029</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Avirulence Protein (AVR)</Keyword><Keyword MajorTopicYN="N">PAMPs (Pathogen Associated Molecular Patterns)</Keyword><Keyword MajorTopicYN="N">PTGS (Post Transcriptional Gene Silencing)</Keyword><Keyword MajorTopicYN="N">RNA silencing</Keyword><Keyword MajorTopicYN="N">innate immunity</Keyword><Keyword MajorTopicYN="N">plant defense</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>04</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>06</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>06</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2021</Year><Month>03</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>10</Month><Day>23</Day><Hour>5</Hour><Minute>57</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>10</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>24</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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