IDL6-HAE/HSL2 impacts pectin degradation and resistance to Pseudomonas syringae pv tomato DC3000 in Arabidopsis leaves
IDL6-HAE/HSL2 impacts pectin degradation and resistance to Pseudomonas syringae pv tomato DC3000 in Arabidopsis leaves
复制标题
IDL6-HAE/HSL2 影响拟南芥叶片中的果胶降解和对番茄番茄 DC3000 假单胞菌的抗性
DOI：
10.1111/tpj.13380
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发表时间：
2017
期刊：
影响因子：
7.2
通讯作者：
Zhang W
中科院分区：
文献类型：
--
作者：
Wang Xin;Hou Shuguo;Wu Qiqi;Lin Minyan;Zhang Wei;Wu Daoji;Acharya Biswa R.;Zhang W
植物细胞壁在发育和生长过程中经历动态的结构和化学变化。花器官脱落和侧根出现都伴随着细胞壁重塑，这涉及脱落中的开花缺乏（IDA）衍生肽及其受体，HAESA（HAE）和HAESA样2（HSL 2）。植物细胞壁也是抵抗病原入侵者的屏障。因此，植物发育过程中的细胞壁重塑可能会影响植物对植物病原体的抗性。在这里，我们鉴定了IDA样6（IDL 6），一个在拟南芥叶片中显著表达的基因。当植物遭受细菌假单胞菌的攻击时，拟南芥叶片中IDL 6的表达显著上调。IDL 6过表达和敲除株系分别降低和提高了拟南芥对PstDC 3000的抗性，表明该基因促进了拟南芥对PstDC 3000的易感性。此外，IDL 6还能促进多聚半乳糖醛酸酶（PG）基因ADPG 2的表达，增加PG活性，从而降低叶片果胶含量和叶片健壮性; ADPG 2过表达抑制拟南芥对PstDC 3000的抗性，而ADPG 2功能缺失突变体则增加对细菌的抗性; PstDC 3000感染部分通过HAE和HSL 2提高ADPG 2的表达。综上所述，我们的结果表明，IDL 6-HAE/HSL 2通过促进拟南芥叶片中的果胶降解来促进PstDC 3000的进入，并且PstDC 3000可能通过操纵IDL 6-HAE/HSL 2-ADPG 2信号通路来增强其感染。
Plant cell walls undergo dynamic structural and chemical changes during plant development and growth. Floral organ abscission and lateral root emergence are both accompanied by cell‐wall remodeling, which involves the INFLORESCENCE DEFICIENT IN ABSCISSION (IDA)‐derived peptide and its receptors, HAESA (HAE) and HAESA‐LIKE2 (HSL2). Plant cell walls also act as barriers against pathogenic invaders. Thus, the cell‐wall remodeling during plant development could have an influence on plant resistance to phytopathogens. Here, we identifiedIDA‐like 6 (IDL6), a gene that is prominently expressed in Arabidopsis leaves.IDL6expression in Arabidopsis leaves is significantly upregulated when the plant is suffering from attacks of the bacterialPseudomonas syringaepv. tomato (Pst) DC3000.IDL6overexpression and knockdown lines respectively decrease and increase the Arabidopsis resistance toPstDC3000, indicating that the gene promotes the Arabidopsis susceptibility toPstDC3000. Moreover,IDL6promotes the expression of a polygalacturonase (PG) gene,ADPG2, and increases PG activity in Arabidopsis leaves, which in turn reduces leaf pectin content and leaf robustness.ADPG2overexpression restrains Arabidopsis resistance toPstDC3000, whereasADPG2loss‐of‐function mutants increase the resistance to the bacterium.PstDC3000 infection elevates theADPG2expression partially through HAE and HSL2. Taken together, our results suggest that IDL6‐HAE/HSL2 facilitates the ingress ofPstDC3000 by promoting pectin degradation in Arabidopsis leaves, andPstDC3000 might enhance its infection by manipulating the IDL6‐HAE/HSL2‐ADPG2 signaling pathway.