the arabidopsis resistance-like gene snc1 is activated by mutations in srfr1 and contributes to resistance to the bacterial effector avrrps4拟南芥抵抗基因snc1由srfr1突变激活,有助于抵抗细菌效应avrrps4.pdfVIP

下载本文档

11
0
约10.5万字
约 14页
2017-09-12 发布于上海
举报
版权申诉

the arabidopsis resistance-like gene snc1 is activated by mutations in srfr1 and contributes to resistance to the bacterial effector avrrps4拟南芥抵抗基因snc1由srfr1突变激活,有助于抵抗细菌效应avrrps4.pdf

1、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。。
2、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
3、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
4、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
5、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
6、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
7、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

the arabidopsis resistance-like gene snc1 is activated by mutations in srfr1 and contributes to resistance to the bacterial effector avrrps4拟南芥抵抗基因snc1由srfr1突变激活,有助于抵抗细菌效应avrrps4

The Arabidopsis Resistance-Like Gene SNC1 Is Activated by Mutations in SRFR1 and Contributes to Resistance to the Bacterial Effector AvrRps4 1. 1. 1 2 3 1 Sang Hee Kim , Fei Gao , Saikat Bhattacharjee , Joseph A. Adiasor , Ji Chul Nam , Walter Gassmann * 1 Division of Plant Sciences, Christopher S. Bond Life Sciences Center and Interdisciplinary Plant Group, University of Missouri, Columbia, Missouri, United States of America, 2 Department of Chemistry, University of Missouri, Columbia, Missouri, United States of America, 3 Division of Biological Sciences, University of Missouri, Columbia, Missouri, United States of America Abstract The SUPPRESSOR OF rps4-RLD1 (SRFR1) gene was identified based on enhanced AvrRps4-triggered resistance in the naturally susceptible Arabidopsis accession RLD. No other phenotypic effects were recorded, and the extent of SRFR1 involvement in regulating effector-triggered immunity was unknown. Here we show that mutations in SRFR1 in the accession Columbia-0 (Col-0) lead to severe stunting and constitutive expression of the defense gene PR1. These phenotypes were temperature- dependent. A cross between srfr1-1 (RLD background) and srfr1-4 (Col-0) showed that stunting was caused by a recessive locus in Col-0. Mapping and targeted crosses identified the Col-0-specific resistance gene SNC1 as the locus that causes stunting. SRFR1 was proposed to function as a transcriptional repressor, and SNC1 is indeed overexpressed in srfr1-4. Interestingly, co-regulated genes in the SNC1 cluster are also upregulated in the srfr1-4 snc1-11 double mutant, indicating that the overexpression of SNC1 is not a secondary effect of constitutive defense activation