维普中文期刊产品整合服务

Arabidopsis small ubiquitin-related modifier protease ASP1 positively regulates abscisic acid signaling during early seedling development~~

查看全文 作  者:Qiongli [1,2]wang;Gao-Ping [1,2]Qu;Xiangxiong [1,2]Kong;Yan [3]Yan;Jigang [3]Li;Jing Bo [1]Jin 高影响力作者 机构地区:[1]Key Laboratory of Plant Molecular Physiology,Institute of Botany,the Chinese Academy of Sciences,Beijing 1ooo93,China;[2]University of the Chinese Academy of Sciences,Beijing 100049,China;[3]State Key Laboratory of Plant Physiology and Biochemistry,College of Biological Sciences,China Agricultural University,Beijing 100193,China高影响力机构 出  处:《Journal of Integrative Plant Biology》索引2018年第60卷第10期,共14页高影响力期刊 基  金:supported by grants from the National Natural Science Foundation of China(31670186);the Chinese Academy of Sciences(XDA08010105) 摘  要:The small ubiquitin-related modifier(SUMO)modification plays an important role in the regulation of abscisic acid(ABA)signaling,but the function of the SUMO protease,in ABA signaling,remains largely unknown.Here,we show that the SUMO protease,ASP1 positively regulates ABA signaling.Mutations in ASP1 resulted in an ABA-insensitive phenotype,during early seedling development.Wild-type ASP1 successfully rescued,whereas an ASP1 mutant(C577S),defective in SUMO protease activity,failed to rescue,the ABA-insensitive phenotype of asp1-1.Expression of ABI5 and MYB30 target genes was attenuated in asp1-1 and our genetic analyses revealed that ASP1 may function upstream of ABI5 and MYB30.Interestingly,ASP1 accumulated upon ABA treatment,and ABA-induced accumulation of ABI5(a positive regulator of ABA signaling)was abolished,whereas ABA-induced accumulation of MYB30(a negative regulator of ABA signaling)was increased in asp1-1.These findings support the hypothesis that increased levels of ASP1,upon ABA treatment,tilt the balance between ABI5 and MYB30towards ABI5-mediated ABA signaling. 关 键 词:ARABIDOPSIS 幼苗期 信号 酶活 修饰 调整 ASPI SUMO
相关文献

参考文献(51)

引证文献(5)

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1 渝公网安备 50019002500403号 违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费