Cytotoxic function of xylanase VdXyn4 in the plant vascular wilt pathogen Verticillium dahliae.
Cytotoxic function of xylanase VdXyn4 in the plant vascular wilt pathogen Verticillium dahliae.
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木聚糖酶 VdXyn4 在植物维管束枯萎病菌大丽黄萎病中的细胞毒功能
DOI：
10.1093/plphys/kiab274
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发表时间：
2021-09-04
期刊：
影响因子：
7.4
通讯作者：
Zhang DD
中科院分区：
文献类型：
--
作者：
Wang D;Chen JY;Song J;Li JJ;Klosterman SJ;Li R;Kong ZQ;Subbarao KV;Dai XF;Zhang DD
植物病原体木聚糖酶在发病机制中发挥着关键作用，这可能是由于它们能够降解植物结构屏障和操纵宿主免疫力。作为植物木质部导管的入侵者，真菌大丽黄萎病被认为能够利用复杂的细胞壁降解酶。比较基因组学分析表明，大丽花基因组编码六种木聚糖酶家族，每种木聚糖酶都具有糖基水解酶 11 结构域，但这些酶的功能尚未确定。基因缺失突变体的表征表明，只有大丽弧菌木聚糖酶 4 (VdXyn4) 能够降解植物细胞壁并增强大丽弧菌的毒力。 VdXyn4 在感染后期表现出细胞毒性活性并诱导坏死表型，导致静脉和叶柄塌陷，这取决于该酶同时定位于细胞核和叶绿体。 VdXyn4 的内化与 BIR1-1 (SOBIR1)/LRR-RLK BRI1 相关激酶 1 (BAK1) 的质膜复合体富含亮氨酸重复序列 (LRR) 受体样激酶抑制因子的内化结合在一起，但我们不能排除 VdXyn4 也可能充当质外体效应子的可能性。相对于已知免疫效应子诱导的免疫信号传导，VdXyn4 诱导的免疫信号传导（在 SA-JA 途径中）明显延迟。虽然细胞毒活性可以被已知的效应子部分抑制，但它们无法阻止本塞姆氏烟草的坏死。因此，与典型的效应器不同，VdXyn4 的细胞毒性在大丽弧菌感染和定植的后期发挥着至关重要的细胞内作用，特别是在病原体进入木质部之后；这种细胞毒活性可能在植物维管病原体的相应酶家族中保守。凭借其细胞毒性活性，大丽轮枝菌木聚糖酶可诱导坏死，导致静脉和叶柄塌陷，这取决于酶同时定位于细胞核和叶绿体。
Phytopathogen xylanases play critical roles in pathogenesis, likely due to their ability to degrade plant structural barriers and manipulate host immunity. As an invader of plant xylem vessels, the fungus Verticillium dahliae is thought to deploy complex cell wall degrading enzymes. Comparative genomics analyses revealed that the V. dahliae genome encodes a family of six xylanases, each possessing a glycosyl hydrolase 11 domain, but the functions of these enzymes are undetermined. Characterizing gene deletion mutants revealed that only V. dahliae xylanase 4 (VdXyn4) degraded the plant cell wall and contributed to the virulence of V. dahliae. VdXyn4 displayed cytotoxic activity and induced a necrosis phenotype during the late stages of infection, leading to vein and petiole collapse that depended on the enzyme simultaneously localizing to nuclei and chloroplasts. The internalization of VdXyn4 was in conjunction with that of the plasma membrane complexLeucine-rich repeat (LRR)-receptor-like kinase suppressor of BIR1-1 (SOBIR1)/LRR-RLK BRI1-associated kinase-1 (BAK1), but we could not rule out the possibility that VdXyn4 may also act as an apoplastic effector. Immune signaling (in the SA–JA pathways) induced by VdXyn4 relative to that induced by known immunity effectors was substantially delayed. While cytotoxic activity could be partially suppressed by known effectors, they failed to impede necrosis in Nicotiana benthamiana. Thus, unlike typical effectors, cytotoxicity of VdXyn4 plays a crucial intracellular role at the late stages of V. dahliae infection and colonization, especially following pathogen entry into the xylem; this cytotoxic activity is likely conserved in the corresponding enzyme families in plant vascular pathogens. By virtue of its cytotoxic activity, Verticillium dahliae Xylanase induces necrosis, leading to vein and petiole collapse that depends on the enzyme simultaneously localizing to nuclei and chloroplasts.
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影响因子：
64.8
作者：
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通讯作者：
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影响因子：
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