Two Host Cytoplasmic Effectors Are Required for Pathogenesis of Phytophthora sojae by Suppression of Host Defenses

Two Host Cytoplasmic Effectors Are Required for Pathogenesis of Phytophthora sojae by Suppression of Host Defenses
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通过抑制宿主防御,大豆疫霉的发病机制需要两个宿主细胞质效应子

DOI:
10.1104/pp.110.166470
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发表时间:
2011-01-01
期刊:
影响因子:
7.4
通讯作者:
Dou, Daolong
Dou, Daolong
中科院分区:
生物学1区
文献类型:
--
作者:
Liu, Tingli;Ye, Wenwu;Dou, Daolong

文献摘要

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大豆疫霉编码数百种具有保守FLAK基序的宿主细胞质效应子,称为皱缩和坏死诱导蛋白(CRN)或Crinkler。它们在发病中的作用和机制大多是未知的。在这里,我们确定了一组五个大豆疫霉特异性CRN样基因具有高水平的序列相似性,其中三个是假定的假基因。功能分析表明,这两个功能基因编码的蛋白质与预测的核定位信号,诱导对比反应时,在本氏烟草和大豆(大豆)。PsCRN63诱导细胞死亡,而PsCRN115抑制由大豆疫霉坏死诱导蛋白(PsojNIP)或PsCRN63引起的细胞死亡。具有缺失的信号肽和FLAK基序的CRN片段的表达证明PsCRN63或PsCRN115的羧基末端部分足以用于它们的活性。然而,预测的核定位信号是PsCRN63诱导细胞死亡所必需的,而不是PsCRN115抑制细胞死亡所必需的。此外,大豆疫霉稳定转化体中PsCRN63和PsCRN115基因的沉默导致对大豆的毒力降低。有趣的是,沉默的转化体失去了抑制接种植物上宿主细胞死亡和胼胝质沉积的能力。这些结果表明CRN效应子在抑制宿主防御反应中的作用。
Phytophthora sojae encodes hundreds of putative host cytoplasmic effectors with conserved FLAK motifs following signal peptides, termed crinkling-and necrosis-inducing proteins (CRN) or Crinkler. Their functions and mechanisms in pathogenesis are mostly unknown. Here, we identify a group of five P. sojae-specific CRN-like genes with high levels of sequence similarity, of which three are putative pseudogenes. Functional analysis shows that the two functional genes encode proteins with predicted nuclear localization signals that induce contrasting responses when expressed in Nicotiana benthamiana and soybean (Glycine max). PsCRN63 induces cell death, while PsCRN115 suppresses cell death elicited by the P. sojae necrosis-inducing protein (PsojNIP) or PsCRN63. Expression of CRN fragments with deleted signal peptides and FLAK motifs demonstrates that the carboxyl-terminal portions of PsCRN63 or PsCRN115 are sufficient for their activities. However, the predicted nuclear localization signal is required for PsCRN63 to induce cell death but not for PsCRN115 to suppress cell death. Furthermore, silencing of the PsCRN63 and PsCRN115 genes in P. sojae stable transformants leads to a reduction of virulence on soybean. Intriguingly, the silenced transformants lose the ability to suppress host cell death and callose deposition on inoculated plants. These results suggest a role for CRN effectors in the suppression of host defense responses.