Sustained Incompatibility between MAPK Signaling and Pathogen Effectors

被引:21
作者
Lang, Julien [1 ]
Colcombet, Jean [2 ]
机构
[1] Univ Paris Saclay, Inst Plant Sci Paris Saclay IPS2, UEVE, CNRS,INRAE, F-91405 Orsay, France
[2] Univ Paris, Inst Plant Sci Paris Saclay IPS2, UEVE, CNRS,INRAE, F-91405 Orsay, France
关键词
Mitogen-Activated Protein Kinases (MAPK); effectors; plant pathogens; ETI; PTI; phosphocode; ACTIVATED PROTEIN-KINASE; SYSTEMIC ACQUIRED-RESISTANCE; CELL-DEATH; INNATE IMMUNITY; SALICYLIC-ACID; DISEASE RESISTANCE; TRIGGERED IMMUNITY; PHYTOALEXIN BIOSYNTHESIS; ETHYLENE BIOSYNTHESIS; ARABIDOPSIS-THALIANA;
D O I
10.3390/ijms21217954
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In plants, Mitogen-Activated Protein Kinases (MAPKs) are important signaling components involved in developemental processes as well as in responses to biotic and abiotic stresses. In this review, we focus on the roles of MAPKs in Effector-Triggered Immunity (ETI), a specific layer of plant defense responses dependent on the recognition of pathogen effector proteins. Having inspected the literature, we synthesize the current state of knowledge concerning this topic. First, we describe how pathogen effectors can manipulate MAPK signaling to promote virulence, and how in parallel plants have developed mechanisms to protect themselves against these interferences. Then, we discuss the striking finding that the recognition of pathogen effectors can provoke a sustained activation of the MAPKs MPK3/6, extensively analyzing its implications in terms of regulation and functions. In line with this, we also address the question of how a durable activation of MAPKs might affect the scope of their substrates, and thereby mediate the emergence of possibly new ETI-specific responses. By highlighting the sometimes conflicting or missing data, our intention is to spur further research in order to both consolidate and expand our understanding of MAPK signaling in immunity.
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页码:1 / 26
页数:26
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