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Paul Birch

Paul Birch

PaulBirch,professorofPlantPathologyandHeadofDivisionofPlantSciences.Hemainlystudieseffectorproteinsfromthepotatolateblightpathogen,Phytophthorainfestans.P.infestansisanoomycete,aeukaryoticpathogenwithafungus-likelifestylethatdevelopshaustoria-finger-likecellstructuresthatformanintimateinteractionwiththehostplasmamembraneduringtheearlystagesofdisease.HehasshownthathaustoriaareamajorsiteofdeliveryofaclassofproteinscalledRXLReffectors.TheRXLRmotifwithinthesesecretedeffectorsisrequiredfortheirtranslocationinsidehostcells.InthegenomeofP.infestanswepredictthatthereare>425RXLReffectorgenes,demonstratingaremarkablepotentialformanipulationofhostprocesses.HeisdiscoveringthatRXLReffectorsinteractdirectlywitharangeofregulatoryproteinsinthehostcelltosuppressorotherwisemanipulateplantdefences.Incontrast,theRXLRsarealsotargetsforhostresistanceproteinswhichactivateimmuneresponsesthatpreventfurthercolonizationbythepathogen.

http://www.zcmsonline.com/index.php/zkzj/47424.html

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详细介绍

Paul Birch,professor of Plant Pathology and Head of Division of Plant Sciences.He mainly studies effector proteins from the potato late blight pathogen, Phytophthora infestans. P. infestans is an oomycete, a eukaryotic pathogen with a fungus-like lifestyle that develops haustoria - finger-like cell structures that form an intimate interaction with the host plasma membrane during the early stages of disease. He has shown that haustoria are a major site of delivery of a class of proteins called RXLR effectors. The RXLR motif within these secreted effectors is required for their translocation inside host cells. In the genome of P. infestans we predict that there are >425 RXLR effector genes, demonstrating a remarkable potential for manipulation of host processes. He is discovering that RXLR effectors interact directly with a range of regulatory proteins in the host cell to suppress or otherwise manipulate plant defences. In contrast, the RXLRs are also targets for host resistance proteins which activate immune responses that prevent further colonization by the pathogen.