AUTHOR=Yeh Yu-Hung , Chang Yu-Hsien , Huang Pin-Yao , Huang Jing-Bo , Zimmerli Laurent 

TITLE=Enhanced Arabidopsis pattern-triggered immunity by overexpression of cysteine-rich receptor-like kinases

JOURNAL=Frontiers in Plant Science

VOLUME=6

YEAR=2015

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2015.00322

DOI=10.3389/fpls.2015.00322

ISSN=1664-462X

ABSTRACT=<p>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 <italic>Arabidopsis thaliana</italic> 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 <italic>CRK4</italic>, <italic>CRK6</italic>, and <italic>CRK36</italic> demonstrated an enhanced PTI response and were resistant to virulent bacteria <italic>Pseudomonas syringae</italic> pv. <italic>tomato</italic> DC3000. Notably, the flg22-triggered oxidative burst was primed in <italic>CRK4</italic>, <italic>CRK6</italic>, and <italic>CRK36</italic> transgenics and up-regulation of the PTI-responsive gene <italic>FLG22-INDUCED RECEPTOR-LIKE 1 (FRK1)</italic> was potentiated upon flg22 treatment in <italic>CRK4</italic> and <italic>CRK6</italic> overexpression lines or constitutively increased by <italic>CRK36</italic> overexpression. PTI-mediated callose deposition was not affected by overexpression of <italic>CRK4</italic> and <italic>CRK6</italic>, while <italic>CRK36</italic> overexpression lines demonstrated constitutive accumulation of callose. In addition, <italic>Pst</italic> DC3000-mediated stomatal reopening was blocked in <italic>CRK4</italic> and <italic>CRK36</italic> overexpression lines, while overexpression of <italic>CRK6</italic> 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 <italic>CRK4</italic>, <italic>CRK6</italic>, and <italic>CRK36</italic> boosts specific PTI outputs and resistance to bacteria suggest a role for these CRKs in Arabidopsis innate immunity.</p>