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MAP Kinases 3 and 6 control Salicylic Acid signaling by upregulating NLR receptors during Pattern- and Effector-Triggered Immunity.

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Arabidopsis thaliana Mitogen-Activated Protein Kinases 3 and 6 (MPK3/6) are transiently activated during PAMP-Triggered Immunity (PTI) and durably during Effector-Triggered Immunity (ETI). However the functional differences between these two kinds… Click to show full abstract

Arabidopsis thaliana Mitogen-Activated Protein Kinases 3 and 6 (MPK3/6) are transiently activated during PAMP-Triggered Immunity (PTI) and durably during Effector-Triggered Immunity (ETI). However the functional differences between these two kinds of activation kinetics and how they coordinate the two layers of plant immunity remain poorly understood. Here, by suppressor analyses, we demonstrate that ETI-mediating Nucleotide-binding domain Leucine-rich repeat Receptors (NLRs) and the NLR signaling components NDR1 and EDS1 can promote the SA sector of defense downstream of MPK3 activity. Moreover we provide evidence that both sustained and transient MPK3/6 activities positively control the expression of several NLR genes, including AT3G04220 and AT4G11170. We further show that NDR1 and EDS1 also contribute to the upregulations of these two NLRs not only in an ETI context but also in a PTI context. Remarkably, while in ETI, MPK3/6 activities are dependent on NDR1 and EDS1, they are not in PTI, suggesting crucial differences in the two signaling pathways. Finally we demonstrate that expression of the NLR AT3G04220 is sufficient to induce expression of defense genes from the SA branch. Overall this study enlarges our knowledge of MPK3/6 functions during immunity and gives a new insight into the intrication of PTI and ETI.

Keywords: map kinases; triggered immunity; immunity; effector triggered; ndr1 eds1

Journal Title: Journal of experimental botany
Year Published: 2022

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