Plants utilize cell surface-localized pattern recognition receptors (PRRs) to detect pathogen-or damage-associated molecular patterns (PAMP/DAMPs) and initiate pattern-triggered immunity (PTI). Here, we investigated the role of Arabidopsis (Arabidopsis thaliana) BRASSINOSTEROID-SIGNALING KINASE5 (BSK5), a member of the receptor-like cytoplasmic kinase subfamily XII, in PRR-initiated immunity. BSK5 localized to the plant cell periphery, interacted in yeast and in planta with multiple receptor-like kinases, including the ELONGATION FACTOR-TU RECEPTOR (EFR) and PEP1 RECEPTOR1 (PEPR1) PRRs, and was phosphorylated in vitro by PEPR1 and EFR in the kinase activation loop. Consistent with a role in PTI, bsk5 mutant plants displayed enhanced susceptibility to the bacterial pathogen Pseudomonas syringae and to the fungus Botrytis cinerea. Furthermore, bsk5 mutant plants were impaired in several immune responses induced by the elf18, pep1, and flg22 PAMP/DAMPs, including resistance to P. syringae and B. cinerea, production of reactive oxygen species, callose deposition at the cell wall, and enhanced PATHOGENESIS-RELATED1 gene expression. However, bsk5 plants were not affected in PAMP/DAMP activation of mitogen-activated protein kinases and expression of the FLG22-INDUCED RECEPTOR-LIKE KINASE1 or the WRKY domain-containing gene WRKY29. BSK5 variants mutated in the BSK5 myristoylation site, ATP-binding site, and kinase activation loop failed to complement defective PTI phenotypes of bsk5 mutant plants, suggesting that localization to the cell periphery, kinase activity, and phosphorylation by PRRs are critical for the function of BSK5 in PTI. These findings demonstrate that BSK5 plays a role in PTI by interacting with multiple immune receptors.

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GH3 proteins control auxin homeostasis by inactivating excess auxin as conjugates of amino acids and sugars and thereby controlling cellular bioactive auxin. Since auxin regulates many aspects of plant growth and development, regulated expression of these genes offers a mechanism to control various developmental processes. OsMGH3/OsGH3-8 is expressed abundantly in rice florets and is regulated by two related and redundant transcription factors, OsMADS1 and OsMADS6, but its contribution to flower development is not known. We functionally characterize OsMGH3 by overexpression and knock-down analysis and show a partial overlap in these phenotypes with that of mutants in OsMADS1 and OsMADS6. The overexpression of OsMGH3 during the vegetative phase affects the overall plant architecture, whereas its inflorescence-specific overexpression creates short panicles with reduced branching, resembling in part the effects of OsMADS1 overexpression. In contrast, the down-regulation of endogenous OsMGH3 caused phenotypes consistent with auxin overproduction or activated signaling, such as ectopic rooting from aerial nodes. Florets in OsMGH3 knock-down plants were affected in carpel development and pollen viability, both of which reduced fertility. Some of these floret phenotypes are similar to osmads6 mutants. Taken together, we provide evidence for the functional significance of auxin homeostasis and its transcriptional regulation during rice panicle branching and floret organ development.

The molecular mechanisms acting between host recognition of pathogen effectors by nucleotide-binding leucine-rich repeat receptor (NLR) proteins and mitogen-activated protein kinase (MAPK) signaling cascades are unknown. MAPKKKα (M3Kα) activates MAPK signaling leading to programmed cell death (PCD) associated with NLR-triggered immunity. We identified a tomato M3Kα-interacting protein, SlMai1, that has 80% amino acid identity with Arabidopsis brassinosteroid kinase 1 (AtBsk1). SlMai1 has a protein kinase domain and a C-terminal tetratricopeptide repeat domain that interacts with the kinase domain of M3Kα. Virus-induced gene silencing of Mai1 homologs in Nicotiana benthamiana increased susceptibility to Pseudomonas syringae and compromised PCD induced by four NLR proteins. PCD was restored by expression of a synthetic SlMai1 gene that resists silencing. Expression of AtBsk1 did not restore PCD in Mai1-silenced plants, suggesting SlMai1 is functionally divergent from AtBsk1. PCD caused by overexpression of M3Kα or MKK2 was unaffected by Mai1 silencing, suggesting Mai1 acts upstream of these proteins. Coexpression of Mai1 with M3Kα in leaves enhanced MAPK phosphorylation and accelerated PCD. These findings suggest Mai1 is a molecular link acting between host recognition of pathogens and MAPK signaling.

Pattern‐triggered immunity (PTI) is typically initiated in plants by recognition of pathogen‐ or damage‐associated molecular patterns (PAMP/DAMPs) by cell surface‐localized pattern recognition receptors (PRRs). Here, we investigated the role in PTI of Arabidopsis thaliana brassinosteroid‐signalling kinases 7 and 8 (BSK7 and BSK8), which are members of the receptor‐like cytoplasmic kinase subfamily XII. BSK7 and BSK8 localized to the plant cell periphery and interacted in yeast and in planta with FLS2, but not with other PRRs. Consistent with a role in FLS2 signalling, bsk7 and bsk8 single and bsk7,8 double mutant plants were impaired in several immune responses induced by flg22, but not by other PAMP/DAMPs. These included resistance to Pseudomonas syringae and Botrytis cinerea, reactive oxygen species accumulation, callose deposition at the cell wall, and expression of the defence‐related gene PR1, but not activation of MAP kinases and expression of the FRK1 and WRKY29 genes. bsk7, bsk8, and bsk7,8 plants also displayed enhanced susceptibility to P. syringae and B. cinerea. Finally, BSK7 and BSK8 variants mutated in their myristoylation site or in the ATP‐binding site failed to complement defective phenotypes of the corresponding mutants, suggesting that localization to the cell periphery and kinase activity are critical for BSK7 and BSK8 functions. Together, these findings demonstrate that BSK7 and BSK8 play a role in PTI initiated by recognition of flg22 by interacting with the FLS2 immune receptor.