植物学报 ›› 2019, Vol. 54 ›› Issue (2): 168-184.DOI: 10.11983/CBB18219
所属专题: 逆境生物学专辑 (2019年54卷2期)
收稿日期:
2018-10-20
接受日期:
2018-12-29
出版日期:
2019-03-01
发布日期:
2019-09-01
通讯作者:
侯岁稳
基金资助:
Received:
2018-10-20
Accepted:
2018-12-29
Online:
2019-03-01
Published:
2019-09-01
Contact:
Suiwen Hou
摘要: 蛋白磷酸化修饰是植物细胞信号调控的普遍机制。植物-病原微生物互作过程中, 关键调控蛋白的磷酸化状态影响免疫信号的激活。多种病原微生物通过干扰宿主蛋白的磷酸化状态攻击免疫系统, 以提高致病性。该文对植物免疫调控过程中关键元件的磷酸化修饰及其在免疫信号中的调控作用进行了综述。研究植物-病原菌互作过程中关键蛋白的磷酸化修饰, 有助于深入探讨植物-病原微生物互作的分子机理。该文将为寻找广谱抗病的新途径提供理论依据。
刘雅琼,侯岁稳. 蛋白磷酸化修饰在植物-病原微生物互作中的作用研究进展. 植物学报, 2019, 54(2): 168-184.
Yaqiong Liu,Suiwen Hou. Research Progress in Protein Phosphorylation in Plant-pathogen Interactions. Chinese Bulletin of Botany, 2019, 54(2): 168-184.
图1 受体激酶和受体蛋白对免疫信号的识别(1) 拟南芥中, LRR类受体激酶和受体蛋白识别病原微生物蛋白或多肽序列; (2) 拟南芥EGF类受体激酶WAK1识别寡聚半乳糖醛酸; (3) Lectin类受体激酶参与免疫信号识别; (4) 拟南芥和水稻LysM类受体激酶或受体蛋白识别几丁质和肽聚糖。
Figure 1 Recognition of the immune signals by receptor kinases and receptor proteins(1) In Arabidopsis, LRR-type receptor kinase and receptor protein recognize pathogenic protein or polypeptide; (2) EGF-type receptor WAK1 recognize oligogalacturonides (OGs); (3) Lectin-type receptor kinase participate in immune signaling recognition; (4) LysM-type receptor kinase or receptor protein recognize chitin and peptidoglycan (PGN) signal in Arabidopsis and rice.
图2 植物中防御相关蛋白的磷酸化修饰调控免疫信号途径(1) 拟南芥中, 未接受病原信号时, PP2A负调控BAK1的激活, 同时BIK1的活性受到PP2C38和CPK28的共同抑制。(2), (3) 病原菌侵染时, LRR类PRRs识别PAMPs, 结合BAK1后被磷酸化激活, LysM类受体激酶CERK1结合LYKs激活免疫信号。(4) 激活的PRRs磷酸化激活胞质内受体激酶(BIK1和PBL27)等。(5) BIK1与CPKs共同磷酸化激活RBOHD, 促进ROS的产生。(6), (7) 激活的RLCKs将信号传递至MAPK信号级联, 导致MAPK激酶被激活。激活的MAPK磷酸化修饰不同的下游底物, 调控不同的防御应答。(8) MKP1、MKP2、PTP1以及AP2C1等磷酸酶负调控MAPKs的活性。(9) 病原菌分泌的效应蛋白HopF2和HopAI1抑制MAPK信号级联途径。(10) 抗病蛋白SUMM2通过监测MPK4对底物MEKK2、CRCK3以及PAT1的磷酸化修饰, 适时地激活ETI途径。
Figure 2 Phosphorylation of defense related proteins in plant immune signaling pathway(1) In Arabidopsis, PP2A negatively regulates the activation of BAK1, meanwhile PP2C38 and CPK28 negatively regulate the phosphorylation of BIK1 without pathogen infection. (2), (3) LRR-type PRRs combine with BAK1 and LysM-type RLK CERK1 combine with LYKs to activate immune signaling after perception of pathogen attack. (4) Activated PRRs phosphorylate BIK1 or PBL27. (5) BIK1 and CPKs phosphorylate RBOHD to promote ROS generation. (6), (7) MAPK cascades are activated and then phosphorylate different substrates to regulate different defense responses. (8) MKP1, MKP2, PTP1 and AP2C1 negatively regulate the activity of MAPKs. (9) Bacterial pathogens inject effector proteins HopF2 and HopAI1 to inhibit the activation of MAPK cascades. (10) Resistance protein SUMM2 activate ETI pathway in time by monitoring the phosphorylation statue of MEKK2, CRCK3 and PAT1, the substrates of MPK4.
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