Plasmodium falciparum and Hyaloperonospora parasitica effector translocation motifs are functional in Phytophthora infestans

Plasmodium falciparum and Hyaloperonospora parasitica effector translocation motifs are functional in Phytophthora infestans
复制标题

DOI:
10.1099/mic.0.2008/021964-0
复制
发表时间:
2008-12-01
期刊:
影响因子:
2.8
通讯作者:
Whisson, Stephen C.
Whisson, Stephen C.
中科院分区:
生物学4区
文献类型:
--
作者:
Grouffaud, Severine;van West, Pieter;Whisson, Stephen C.

文献摘要

被引文献

相似文献

卵菌纲马铃薯晚疫病病原体致病疫霉和顶复门疟疾寄生虫恶性疟原虫在宿主细胞内转运效应蛋白,可能是为了病原体或寄生虫的利益。许多卵菌候选分泌效应蛋白具有一个肽结构域,其核心保守基序RxLR位于N-末端分泌信号肽附近。在致病疫霉效应子Avr 3a中,RxLR和另外的EER基序对于在感染期间易位到宿主细胞中是必需的。Avr 3a在宿主细胞质中被R3 a抗性蛋白识别。我们已经利用这种细胞质识别来报道Avr 3a的RxLR-EER被来自相关卵菌病原体Hyaloperotiospora parasitica的细胞内效应物ATR 1 NdWsB和ATR 13的等同序列以及来自Pl的宿主靶向信号替代。恶性疟原虫毒力蛋白PfHRPII。将这些嵌合转基因引入致病疫霉中并随后在表达R3 a的马铃薯植物上进行毒力测试,证明了替代基序在植物细胞内易位Avr 3a中具有功能。这些结果表明,在疟疾和卵菌病理系统的蛋白质易位的共同机制。
The oomycete potato late blight pathogen, Phytophthora infestans, and the apicomplexan malaria parasite Plasmodium falciparum translocate effector proteins inside host cells, presumably to the benefit of the pathogen or parasite. Many oomycete candidate secreted effector proteins possess a peptide domain with the core conserved motif, RxLR, located near the N-terminal secretion signal peptide. In the Ph. infestans effector Avr3a, RxLR and an additional EER motif are essential for translocation into host cells during infection. Avr3a is recognized in the host cytoplasm by the R3a resistance protein. We have exploited this cytoplasmic recognition to report on replacement of the RxLR-EER of Avr3a with the equivalent sequences from the intracellular effectors ATR1NdWsB and ATR13 from the related oomycete pathogen, Hyaloperotiospora parasitica, and the host targeting signal from the Pl. falciparum virulence protein PfHRPII. Introduction of these chimeric transgenes into Ph. infestans and subsequent virulence testing on potato plants expressing R3a demonstrated the alternative motifs to be functional in translocating Avr3a inside plant cells. These results suggest common mechanisms for protein translocation in both malaria and oomycete pathosystems.