A conserved module regulates receptor kinase signalling in immunity and development

DeFalco, Thomas A.; Anne, Pauline; James, Sean R.; Willoughby, Andrew; Schwanke, Florian; Johanndrees, Oliver; Genolet, Yasmine; Derbyshire, Paul; Wang, Qian; Rana, Surbhi; Pullen, Anne-Marie; Menke, Frank L.H.; Zipfel, Cyril; Hardtke, Christian S.; Nimchuk, Zachary L.

doi:10.1038/s41477-022-01134-w

Cited by 40 publications

(24 citation statements)

References 53 publications

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“…4c, d). These data suggest that, surprisingly, brx is genetically epistatic to pbl34/35/36, although pbl34/35/36 triple mutants are strongly resistant to CLE45 38,39 . This can be understood by our observation that brx loss-of-function conferred renewed albeit reduced CLE45 sensitivity both in bam3 brx double mutant and brx pbl34/35/36 quadruple mutant backgrounds (Fig.…”

Section: Effectors Of Cle45 Signaling Directly Interact With a Rheost...mentioning

confidence: 87%

“…Interestingly, triple knock-out of the redundant downstream CLE peptide signaling components PBL34, PBL35 and PBL36 cannot rescue the visible differentiation defects in brx mutants (Fig. 4a) 38,39 , but slightly promotes root growth in both wildtype and brx background (Fig. 4b).…”

Section: Effectors Of Cle45 Signaling Directly Interact With a Rheost...mentioning

confidence: 99%

“…Because higher order mutants of PBL34/35/36-related receptor-like cytoplasmic kinases (RLCKs) do not display any marked resistance to various CLE peptides including CLE45 (Supplementary Fig. 5i) 38 , alternative downstream effectors may also be involved. However, our findings also indicate that PBL34/35/36 signaling represents a branched output of CLE45-BAM3 signaling because brx pbl34/35/36 mutants were considerably more sensitive to CLE45 treatment than bam3 brx mutants (Fig.…”

Section: Effectors Of Cle45 Signaling Directly Interact With a Rheost...mentioning

confidence: 99%

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A phosphoinositide hub connects CLE peptide signaling and polar auxin efflux regulation

et al. 2023

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Auxin efflux through plasma-membrane-integral PIN-FORMED (PIN) carriers is essential for plant tissue organization and tightly regulated. For instance, a molecular rheostat critically controls PIN-mediated auxin transport in developing protophloem sieve elements of Arabidopsis roots. Plasma-membrane-association of the rheostat proteins, BREVIS RADIX (BRX) and PROTEIN KINASE ASSOCIATED WITH BRX (PAX), is reinforced by interaction with PHOSPHATIDYLINOSITOL-4-PHOSPHATE-5-KINASE (PIP5K). Genetic evidence suggests that BRX dampens autocrine signaling of CLAVATA3/EMBRYO SURROUNDING REGION-RELATED 45 (CLE45) peptide via its receptor BARELY ANY MERISTEM 3 (BAM3). How excess CLE45-BAM3 signaling interferes with protophloem development and whether it does so directly or indirectly remains unclear. Here we show that rheostat polarity is independent of PIN polarity, but interdependent with PIP5K. Catalytically inactive PIP5K confers rheostat polarity without reinforcing its localization, revealing a possible PIP5K scaffolding function. Moreover, PIP5K and PAX cooperatively control local PIN abundance. We further find that CLE45-BAM3 signaling branches via RLCK-VII/PBS1-LIKE (PBL) cytoplasmic kinases to destabilize rheostat localization. Our data thus reveal antagonism between CLE45-BAM3-PBL signaling and PIP5K that converges on auxin efflux regulation through dynamic control of PAX polarity. Because second-site bam3 mutation suppresses root as well as shoot phenotypes of pip5k mutants, CLE peptide signaling likely modulates phosphoinositide-dependent processes in various developmental contexts.

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Section: Effectors Of Cle45 Signaling Directly Interact With a Rheost...mentioning

confidence: 87%

Section: Effectors Of Cle45 Signaling Directly Interact With a Rheost...mentioning

confidence: 99%

Section: Effectors Of Cle45 Signaling Directly Interact With a Rheost...mentioning

confidence: 99%

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A phosphoinositide hub connects CLE peptide signaling and polar auxin efflux regulation

et al. 2023

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“…Interestingly, PP2C38 S77 (feedback) phosphorylation by its own substrate, BIK1, is needed for BIK1-PP2C38 dissociation from the PRR complex. Recent data also pinpoint similar mechanism for additional PP2Cs, namely poltergeist-like 4 and 5 (PLL4 & 5) where PLL4 dissociation is preceded by phosphorylation through BIK1 [ 79 ].…”

Section: Rewriting the Immune Phosphocode Through Protein Phosphatase...mentioning

confidence: 98%

What’s new in protein kinase/phosphatase signalling in the control of plant immunity?

Erickson

Weckwerth

Romeis

et al. 2022

Essays in Biochemistry

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Plant immunity is crucial to plant health but comes at an expense. For optimal plant growth, tight immune regulation is required to prevent unnecessary rechannelling of valuable resources. Pattern- and effector-triggered immunity (PTI/ETI) represent the two tiers of immunity initiated after sensing microbial patterns at the cell surface or pathogen effectors secreted into plant cells, respectively. Recent evidence of PTI-ETI cross-potentiation suggests a close interplay of signalling pathways and defense responses downstream of perception that is still poorly understood. This review will focus on controls on plant immunity through phosphorylation, a universal and key cellular regulatory mechanism. Rather than a complete overview, we highlight “what’s new in protein kinase/phosphatase signalling” in the immunity field. In addition to phosphoregulation of components in the pattern recognition receptor (PRR) complex, we will cover the actions of the major immunity-relevant intracellular protein kinases/phosphatases in the ‘signal relay’, namely calcium-regulated kinases (e.g. calcium-dependent protein kinases, CDPKs), mitogen-activated protein kinases (MAPKs), and various protein phosphatases. We discuss how these factors define a phosphocode that generates cellular decision-making ‘logic gates’, which contribute to signalling fidelity, amplitude, and duration. To underscore the importance of phosphorylation, we summarize strategies employed by pathogens to subvert plant immune phosphopathways. In view of recent game-changing discoveries of ETI-derived resistosomes organizing into calcium-permeable pores, we speculate on a possible calcium-regulated phosphocode as the mechanistic control of the PTI-ETI continuum.

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“…pol mutations are known to repress stem cell defects in diverse clv class mutants to varying degrees 43,44 . We recently discovered that POL dampens CLEp signaling by dephosphorylating CLV1/BAM class receptors, providing a mechanistic explanation for POL function 45 . Therefore, we asked if ectopic CLV1 signaling was responsible for the restoration of primordia outgrowth in crn pol plants.…”

Section: Mainmentioning

confidence: 99%

A network of CLAVATA receptors buffers auxin-dependent meristem maintenance

John

Smith

Jones

et al. 2022

Preprint

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Plant body plans are elaborated in response to both environmental and endogenous cues. How these inputs intersect to promote growth and development remains poorly understood. During reproductive development, central zone stem cell proliferation in inflorescence meristems is negatively regulated by the CLAVATA3 (CLV3) peptide signaling pathway. In contrast, floral primordia formation on meristem flanks requires the hormone auxin. Here we show that CLV3 signaling is also necessary for auxin-dependent floral primordia generation and that this function is partially masked by both inflorescence fasciation and heat-induced auxin biosynthesis. Stem cell regulation by CLAVATA signaling is separable from primordia formation but is also sensitized to temperature and auxin levels. Additionally, we uncover a novel role for the CLV3 receptor CLAVATA1 in auxin-dependent meristem maintenance in cooler environments. As such, CLV3 signaling buffers multiple auxin-dependent shoot processes across divergent thermal environments with opposing effects on cell proliferation in different meristem regions.

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A conserved module regulates receptor kinase signalling in immunity and development

Cited by 40 publications

References 53 publications

A phosphoinositide hub connects CLE peptide signaling and polar auxin efflux regulation

A phosphoinositide hub connects CLE peptide signaling and polar auxin efflux regulation

What’s new in protein kinase/phosphatase signalling in the control of plant immunity?

A network of CLAVATA receptors buffers auxin-dependent meristem maintenance

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