Disease Resistance Through Infection Site Production of a Toxic α-SNAP that Impairs Vesicle Trafficking
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- 英文论文题名：Disease Resistance Through Infection Site Production of a Toxic α-SNAP that Impairs Vesicle Trafficking
- 论文作者：Andrew Bent
- 英文论文作者：Andrew Bent ; Professor ; Department of Plant Pathology ; University of Wisconsin-Madison
- 年：2016
- 作者机构：Professor,Department of Plant Pathology,University of Wisconsin-Madison;
- 会议召开时间：2016-08-05
- 会议录名称：中国植物病理学会2016年学术年会论文集
- 英文会议录名称：Proceedings of the Annual Meeting of Chinese Society for Plant Pathology(2016)
- 语种：英文
- 分类号：S432.23
- 学会代码：ZGVS
- 会议名称：中国植物病理学会2016年学术年会
- 会议地点：中国江苏南京
- 主办单位：中国植物病理学会
- 学会名称：中国植物病理学会
- 页数：1
- 文件大小：58k
- 原文格式：O
- 会议级别：全国
摘要
Current paradigms for mechanisms of plant disease resistance emphasize expression of R gene products or MAMP receptors that mediate pathogen detection,causing cell wall reinforcement,production of antimicrobial compounds,and in some cases,hypersensitive response(HR) cell death.Paradigms are less well developed for mechanisms of plant defense against biotrophic pathogens that overcome preformed plant defenses,escape detection by R gene products,and secrete effectors that block other typical plant immune responses.We have identified at least part of the mechanism for soybeanRhg1,a complex locus that confers resistance to soybean cyst nematode(SCN).Soybean is one of the world's four largest food crops.SCN is by far the most yield-reducing pathogen of soybean in the U.S.SCN often does not cause obvious above-ground disease symptoms,so many growers do not try enough to fight this disease.SCN is also one of the most damaging pathogens of soybean in China.SCN invade plant roots and establish a feeding site called a "syncitium" near the root vascular cylinder.This feeding site takes over and massively reprograms multiple surrounding root cells.For successful growth and reproduction,SCN must keep plant syncitium cells active and cooperative for at least three weeks.Rhg1 is widely used by plant breeders and soybean farmers to control SCN,and Rhg1 has been known for many years to function by causing early failure of the developing syncitium.We first reported in 2012 that one of the Rhg1 genes causing SCN resistance encodes an unusual alpha-SNAP protein.α-SNAP functions with NSF(an ATPase) to mediate vesicle trafficking by forming the core SNARE recycling machinery.α-SNAPs are conserved across eukaryotes.α-SNAP stimulates SNARE complex disassembly by NSF,which enables future rounds of vesicle fusion.We now have evidence that the soybean Rhg1 α-SNAP interacts less well with NSF,impairs exocytosis and other vesicular trafficking,and is cytotoxic at high doses.This toxicity is dose-dependent,and can be prevented by shifting the cellular ratio toward wild-typeα-SNAPs.Rhg1 α-SNAP levels increase in the SCN-induced syncitium.Hence this very important disease resistance functions by an interesting mechanism:the host carries a toxic variant of a core housekeeping protein,the abundance of the protein is low enough in most tissues to not harm plant yields,but the biotrophic interface established by the pathogen is disrupted by elevated abundance of the protein,which in the case of Rhg1 disrupts cellular vesicle trafficking.
Current paradigms for mechanisms of plant disease resistance emphasize expression of R gene products or MAMP receptors that mediate pathogen detection,causing cell wall reinforcement,production of antimicrobial compounds,and in some cases,hypersensitive response(HR) cell death.Paradigms are less well developed for mechanisms of plant defense against biotrophic pathogens that overcome preformed plant defenses,escape detection by R gene products,and secrete effectors that block other typical plant immune responses.We have identified at least part of the mechanism for soybeanRhg1,a complex locus that confers resistance to soybean cyst nematode(SCN).Soybean is one of the world's four largest food crops.SCN is by far the most yield-reducing pathogen of soybean in the U.S.SCN often does not cause obvious above-ground disease symptoms,so many growers do not try enough to fight this disease.SCN is also one of the most damaging pathogens of soybean in China.SCN invade plant roots and establish a feeding site called a "syncitium" near the root vascular cylinder.This feeding site takes over and massively reprograms multiple surrounding root cells.For successful growth and reproduction,SCN must keep plant syncitium cells active and cooperative for at least three weeks.Rhg1 is widely used by plant breeders and soybean farmers to control SCN,and Rhg1 has been known for many years to function by causing early failure of the developing syncitium.We first reported in 2012 that one of the Rhg1 genes causing SCN resistance encodes an unusual alpha-SNAP protein.α-SNAP functions with NSF(an ATPase) to mediate vesicle trafficking by forming the core SNARE recycling machinery.α-SNAPs are conserved across eukaryotes.α-SNAP stimulates SNARE complex disassembly by NSF,which enables future rounds of vesicle fusion.We now have evidence that the soybean Rhg1 α-SNAP interacts less well with NSF,impairs exocytosis and other vesicular trafficking,and is cytotoxic at high doses.This toxicity is dose-dependent,and can be prevented by shifting the cellular ratio toward wild-typeα-SNAPs.Rhg1 α-SNAP levels increase in the SCN-induced syncitium.Hence this very important disease resistance functions by an interesting mechanism:the host carries a toxic variant of a core housekeeping protein,the abundance of the protein is low enough in most tissues to not harm plant yields,but the biotrophic interface established by the pathogen is disrupted by elevated abundance of the protein,which in the case of Rhg1 disrupts cellular vesicle trafficking.
Current paradigms for mechanisms of plant disease resistance emphasize expression of R gene products or MAMP receptors that mediate pathogen detection,causing cell wall reinforcement,production of antimicrobial compounds,and in some cases,hypersensitive response(HR) cell death.Paradigms are less well developed for mechanisms of plant defense against biotrophic pathogens that overcome preformed plant defenses,escape detection by R gene products,and secrete effectors that block other typical plant immune responses.We have identified at least part of the mechanism for soybeanRhg1,a complex locus that confers resistance to soybean cyst nematode(SCN).Soybean is one of the world's four largest food crops.SCN is by far the most yield-reducing pathogen of soybean in the U.S.SCN often does not cause obvious above-ground disease symptoms,so many growers do not try enough to fight this disease.SCN is also one of the most damaging pathogens of soybean in China.SCN invade plant roots and establish a feeding site called a "syncitium" near the root vascular cylinder.This feeding site takes over and massively reprograms multiple surrounding root cells.For successful growth and reproduction,SCN must keep plant syncitium cells active and cooperative for at least three weeks.Rhg1 is widely used by plant breeders and soybean farmers to control SCN,and Rhg1 has been known for many years to function by causing early failure of the developing syncitium.We first reported in 2012 that one of the Rhg1 genes causing SCN resistance encodes an unusual alpha-SNAP protein.α-SNAP functions with NSF(an ATPase) to mediate vesicle trafficking by forming the core SNARE recycling machinery.α-SNAPs are conserved across eukaryotes.α-SNAP stimulates SNARE complex disassembly by NSF,which enables future rounds of vesicle fusion.We now have evidence that the soybean Rhg1 α-SNAP interacts less well with NSF,impairs exocytosis and other vesicular trafficking,and is cytotoxic at high doses.This toxicity is dose-dependent,and can be prevented by shifting the cellular ratio toward wild-typeα-SNAPs.Rhg1 α-SNAP levels increase in the SCN-induced syncitium.Hence this very important disease resistance functions by an interesting mechanism:the host carries a toxic variant of a core housekeeping protein,the abundance of the protein is low enough in most tissues to not harm plant yields,but the biotrophic interface established by the pathogen is disrupted by elevated abundance of the protein,which in the case of Rhg1 disrupts cellular vesicle trafficking.
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