SERK5 genetically compensates for the loss of BAK1 and BKK1 in regulating elf18-triggered immune signaling in <i>Arabidopsis</i>.

Abstract

SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASEs (SERKs), particularly BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE 1 (BAK1) (SERK3) and BKK1 (SERK4), function as pleiotropic coreceptors to transduce extracellular developmental and immune signals in <i>Arabidopsis thaliana</i>. However, SERK5, the closest paralog of BAK1/BKK1, is long considered a nonfunctional kinase due to a mutation in the conserved arginine-aspartic acid (RD) motif within its kinase domain. Here, we show that artificial microRNA (amiRNA)-mediated cosilencing of <i>BAK1</i>/<i>BKK1</i>/<i>SERK5</i> induces autoimmunity, which is more severe than that observed in <i>bak1 bkk1</i> double mutants. Complementation with the amiRNA-resistant <i>mSERK5</i>, but surprisingly not with <i>mSERK5Km</i> encoding an ATP-binding-deficient SERK5, rescues this autoimmunity. Knockout of <i>ENHANCED DISEASE SUSCEPTIBILITY 1</i>, a central component of plant immunity with important functions in effector-triggered immunity (ETI), or <i>BAK-TO-LIFE 2</i>, a surveillance protein sensing BAK1/BKK1 perturbations in immunity, partially suppresses the amiRNA-mediated autoimmunity. The bacterial elicitor elf18 swiftly upregulates <i>SERK5</i> expression. <i>BAK1</i>/<i>BKK1</i>/<i>SERK5</i> cosilencing seedlings complemented with <i>mSERK5</i> maintain wild-type levels of elf18-induced mitogen-activated protein kinase (MAPK) activation, while overexpression of <i>SERK5</i>, but not unrelated <i>SERK1</i> or <i>SERK2</i>, restores normal elf18-induced MAPK activation in <i>bak1</i> null protoplasts. These findings unmask a substitute coreceptor role for SERK5 in elf18 signaling, and suggest that plants can monitor and discriminate between concurrent BAK1/BKK1/SERK5 inactivation and BAK1/BKK1 depletion to fine-tune the severity of downstream ETI responses.