Abstract
Upon recognition of microbe-associated molecular patterns (MAMPs) such as the bacterial flagellin (or the derived peptide flg22) by pattern-recognition receptors (PRRs) such as the FLAGELLIN SENSING2 (FLS2), plants activate the pattern-triggered immunity (PTI) response. The L-type lectin receptor kinase-VI.2 (LecRK-VI.2) is a positive regulator of Arabidopsis thaliana PTI. Cysteine-rich receptor-like kinases (CRKs) possess two copies of the C-X8-C-X2-C (DUF26) motif in their extracellular domains and are thought to be involved in plant stress resistance, but data about CRK functions are scarce. Here, we show that Arabidopsis overexpressing the LecRK-VI.2-responsive CRK4, CRK6, and CRK36 demonstrated an enhanced PTI response and were resistant to virulent bacteria Pseudomonas syringae pv. tomato DC3000. Notably, the flg22-triggered oxidative burst was primed in CRK4, CRK6, and CRK36 transgenics and up-regulation of the PTI-responsive gene FLG22-INDUCED RECEPTOR-LIKE 1 (FRK1) was potentiated upon flg22 treatment in CRK4 and CRK6 overexpression lines or constitutively increased by CRK36 overexpression. PTI-mediated callose deposition was not affected by overexpression of CRK4 and CRK6, while CRK36 overexpression lines demonstrated constitutive accumulation of callose. In addition, Pst DC3000-mediated stomatal reopening was blocked in CRK4 and CRK36 overexpression lines, while overexpression of CRK6 induced constitutive stomatal closure suggesting a strengthening of stomatal immunity. Finally, bimolecular fluorescence complementation and co-immunoprecipitation analyses in Arabidopsis protoplasts suggested that the plasma membrane localized CRK4, CRK6, and CRK36 associate with the PRR FLS2. Association with FLS2 and the observation that overexpression of CRK4, CRK6, and CRK36 boosts specific PTI outputs and resistance to bacteria suggest a role for these CRKs in Arabidopsis innate immunity.
Highlights
Cell surface plant receptor-like kinases (RLKs) link perception of environmental stimuli and downstream signal transductions to trigger appropriate intracellular responses
Lines Overexpressing CRK4, CRK6, and CRK36 are More Resistant to Virulent Bacteria Overexpression of LecRK-VI.2, a positive regulator of pattern-triggered immunity (PTI), induces a strong up-regulation (> 10 times) of CRK37 (At4g04500), CRK23 (At4g23310), CRK7 (At4g23150), CRK6 (At4g23140), CRK36 (At4g04490), CRK13 (At4g23210), and CRK4 (At3g45860) (Supplementary Table 2) (Singh et al, 2012a)
To test the possible role of these Cysteine-rich receptor-like kinases (CRKs) in the Arabidopsis resistance response to bacterial pathogens, T-DNA insertion lines were ordered at Arabidopsis Biological Resource Center (ABRC) and homozygotic mutants were tested for their resistance to the virulent bacterial pathogen Pst DC3000
Summary
Cell surface plant receptor-like kinases (RLKs) link perception of environmental stimuli and downstream signal transductions to trigger appropriate intracellular responses. The best-studied RLK sub-family is characterized by the presence of leucine-rich repeat (LRR) motifs in the extracellular region. Members of this sub-family are involved in a wide range of plant signaling initiation and activation processes (Walker, 1994; Kobe and Kajava, 2001). The malectin-like LRR-RLK IMPAIRED OOMYCETE SUSCEPTIBILITY1 (IOS1) enhances PTI through the regulation of FLS2-BAK1 association (Chen et al, 2014). Another LRR-RLK, BAK1-INTERACTING RECEPTOR-LIKE KINASE 2 (BIR2) acts by negatively regulating BAK1 function to maintain immune homeostasis through the control of BAK1-FLS2 complex formation (Halter et al, 2014). Current understanding suggests that PRRs are central components of multiprotein complexes and that a dynamic regulation exists among the members of PRR complexes to fine tune the different PTI outputs (Macho and Zipfel, 2014)
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