Plant Innate Immunity: Perception of Conserved Microbial Signatures

Schwessinger, Benjamin; Ronald, Pamela C.

doi:10.1146/annurev-arplant-042811-105518

Cited by 310 publications

(260 citation statements)

References 226 publications

(264 reference statements)

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“…Most PRRs in the model plant Arabidopsis are involved in plant immunity. 13,4,10,29,40,23 In the plant-pathogen arms race, successful pathogens secrete dozens of effector proteins to modulate host physiology and to undermine PTI, the pathways of which has been well characterized for bacterial and oomycete pathogens. 1,16,17 Bacterial pathogens evolved molecular secretion systems for effector delivery, such as the type-III and type-IV secretion systems, 31 while the delivery and entry of oomycete and fungal effectors into host cells was just started to be understood.…”

Section: Introductionmentioning

confidence: 99%

Botrytis small RNA Bc-siR37 suppresses plant defense genes by cross-kingdom RNAi

et al. 2017

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Pathogens secrete effector proteins to suppress host immune responses. Recently, we showed that an aggressive plant fungal pathogen Botrytis cinerea can also deliver small RNA effectors into host cells to suppress host immunity. B. cinerea sRNAs (Bc-sRNAs) translocate into host plants and hijack the plant RNAi machinery to induce cross-kingdom RNAi of host immune responsive genes. Here, we functionally characterized another Bc-sRNA effector Bc-siR37 that is predicted to target at least 15 Arabidopsis genes, including WRKY transcription factors, receptor-like kinases, and cell wall-modifying enzymes. Upon B. cinerea infection, the expression level of Bc-siR37 was induced, and at least eight predicted Arabidopsis target genes were downregulated. These target genes were also suppressed in the transgenic Arabidopsis plants overexpressing Bc-siR37, which exhibited enhanced disease susceptibility to B. cinerea. Furthermore, the knockout mutants of the Bc-siR37 targets, At-WRKY7, At-PMR6, and At-FEI2, also exhibited enhanced disease susceptibility to B. cinerea, giving further support that these genes indeed play a positive role in plant defense against B. cinerea. Our study demonstrates that analysis of pathogen sRNA effectors can be a useful tool to help identify host immunity genes against the corresponding pathogen.

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Section: Introductionmentioning

confidence: 99%

Botrytis small RNA Bc-siR37 suppresses plant defense genes by cross-kingdom RNAi

et al. 2017

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“…As an early defense response, papilla formation can contribute to the plant's innate immunity (Jones and Dangl, 2006;Schwessinger and Ronald, 2012), which is associated with global transcriptional changes (Boller and Felix, 2009). Plant defense mechanisms that contribute to the innate immunity give the host plant time to initiate subsequent defense reactions that require gene activation and expression, such as the hypersensitive response, phytoalexin production, and the synthesis and export of pathogenesis-related proteins (Lamb and Dixon, 1997;Brown et al, 1998).…”

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confidence: 99%

Elevated Early Callose Deposition Results in Complete Penetration Resistance to Powdery Mildew in Arabidopsis

et al. 2013

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A common response by plants to fungal attack is deposition of callose, a (1,3)-b-glucan polymer, in the form of cell wall thickenings called papillae, at site of wall penetration. While it has been generally believed that the papillae provide a structural barrier to slow fungal penetration, this idea has been challenged in recent studies of Arabidopsis (Arabidopsis thaliana), where fungal resistance was found to be independent of callose deposition. To the contrary, we show that callose can strongly support penetration resistance when deposited in elevated amounts at early time points of infection. We generated transgenic Arabidopsis lines that express POWDERY MILDEW RESISTANT4 (PMR4), which encodes a stress-induced callose synthase, under the control of the constitutive 35S promoter. In these lines, we detected callose synthase activity that was four times higher than that in wild-type plants 6 h post inoculation with the virulent powdery mildew Golovinomyces cichoracearum. The callose synthase activity was correlated with enlarged callose deposits and the focal accumulation of green fluorescent protein-tagged PMR4 at sites of attempted fungal penetration. We observed similar results from infection studies with the nonadapted powdery mildew Blumeria graminis f. sp. hordei. Haustoria formation was prevented in resistant transgenic lines during both types of powdery mildew infection, and neither the salicylic acid-dependent nor jasmonate-dependent pathways were induced. We present a schematic model that highlights the differences in callose deposition between the resistant transgenic lines and the susceptible wild-type plants during compatible and incompatible interactions between Arabidopsis and powdery mildew.Land plants are exposed to a wide range of potential pathogens and, accordingly, have evolved a variety of strategies that facilitate an early and rapid recognition of pathogens and the mobilization of biochemical and structural defenses. As a result, successful infection of plants by pathogens is the exception rather than the rule (

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“…The first layer of innate immunity is activated by sensing of the conserved microbial signatures, termed pathogen-or microbe-associated molecular patterns (PAMPs or MAMPs) by plasma membrane (PM)-resident pattern recognition receptors (PRRs) (3,4). Evidence indicates that PRRs also detect the endogenous molecules derived from damaged cells, termed damage-associated molecular patterns (DAMPs) (3).…”

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confidence: 99%

Tyrosine phosphorylation of protein kinase complex BAK1/BIK1 mediates Arabidopsis innate immunity

Lin¹,

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

161

138

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The sessile plants have evolved a large number of receptor-like kinases (RLKs) and receptor-like cytoplasmic kinases (RLCKs) to modulate diverse biological processes, including plant innate immunity. Phosphorylation of the RLK/RLCK complex constitutes an essential step to initiate immune signaling. Two Arabidopsis plasma membrane-resident RLKs, flagellin-sensing 2 and brassinosteroid insensitive 1-associated kinase 1 (BAK1), interact with RLCK Botrytis-induced kinase 1 (BIK1) to initiate plant immune responses to bacterial flagellin. BAK1 directly phosphorylates BIK1 and positively regulates plant immunity. Classically defined as a serine/threonine kinase, BIK1 is shown here to possess tyrosine kinase activity with mass spectrometry, immunoblot, and genetic analyses. BIK1 is autophosphorylated at multiple tyrosine (Y) residues in addition to serine/threonine residues. Importantly, BAK1 is able to phosphorylate BIK1 at both tyrosine and serine/ threonine residues. BIK1Y150 is likely catalytically important as the mutation blocks both tyrosine and serine/threonine kinase activity, whereas Y243 and Y250 are more specifically involved in tyrosine phosphorylation. The BIK1 tyrosine phosphorylation plays a crucial role in BIK1-mediated plant innate immunity as the transgenic plants carrying BIK1Y150F, Y243F, or Y250F (the mutation of tyrosine to phenylalanine) failed to complement the bik1 mutant deficiency in immunity. Our data indicate that plant RLCK BIK1 is a nonreceptor dual-specificity kinase and both tyrosine and serine/ threonine kinase activities are required for its functions in plant immune signaling. Together with the previous finding of BAK1 to be autophosphorylated at tyrosine residues, our results unveiled the tyrosine phosphorylation cascade as a common regulatory mechanism that controls membrane-resident receptor signaling in plants and metazoans.

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Plant Innate Immunity: Perception of Conserved Microbial Signatures

Cited by 310 publications

References 226 publications

Botrytis small RNA Bc-siR37 suppresses plant defense genes by cross-kingdom RNAi

Botrytis small RNA Bc-siR37 suppresses plant defense genes by cross-kingdom RNAi

Elevated Early Callose Deposition Results in Complete Penetration Resistance to Powdery Mildew in Arabidopsis

Tyrosine phosphorylation of protein kinase complex BAK1/BIK1 mediates Arabidopsis innate immunity

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