BIK1 function in plant growth and defense signaling.

Plant pathogens can be categorized based on their feeding habits, specifically whether they are biotrophic and feed off of living host tissues, or if they are necrotrophic and feed off of dead and decaying tissues. Not surprisingly, when attacked by pathogens with different feeding habits, plants employ different but overlapping defense strategies to limit pathogen growth and disease development. Biotrophic pathogens often induce effector-triggered immunity in host plants, characterized by gene-for-gene resistance, whereby specific effector molecules trigger an R gene response in the host leading to targeted programmed cell death as part of the hypersensitive response, which limits pathogen growth. By contrast, necrotrophs feed off of cell death in the host, making effector-triggered immunity generally an ineffective strategy. Necrotrophic pathogens instead may induce pathogen-associated molecular pattern–triggered immunity (PTI), involving the induction of jasmonate(JA) and ethylene (ET)–dependent pathways that activate a different set of defense responses. These include the induction of camalexin biosynthesis and other responses that limit pathogen growth and the ability of the pathogen to cause host cell death. One of the central components of PTI signaling in Arabidopsis thaliana is BOTRYTISINDUCED KINASE1 (BIK1), which was identified as an early-induced gene in response to infection by Botrytis cinerea. BIK1 is required for resistance to the necrotrophic fungal pathogens B. cinerea and Alternaria brassicicola but suppresses defense against the (hemibiotrophic) bacterial pathogen Pseudomonas syringae (Veronese et al., 2006). BIK1 encodes a receptor-like cytoplasmic kinase that mediates PTI signaling from multiple pathogen-associated molecular pattern receptors (Lu et al., 2010; Zhang et al., 2010). Laluk et al. (pages 2831–2849) present a detailed analysis of the genetic, molecular, and biochemical function of BIK1 in regulating responses to bacterial and fungal pathogens. The authors use site-directed mutagenesis, biochemical assays, and mutant analysis to define specific residues essential for BIK1 phosphorylation, in vivo kinase activity, and biological function (see figure). The results show how differential phosphorylation in the kinase domain region might confer specificity to BIK1 function. They also show that BIK1 is required for seedling growth responses to ET and glucose, which are known to interact antagonistically. BIK1 was found to be required for ET signaling, having a function similar to that of EIN2, a central transducer of ET signaling. Induction of immunity to B. cinerea required both BIK1 and EIN2 but did not involve salicylate responses and was antagonized by COI1 (a key component of JA signaling). By contrast, basal and induced PTI responses to virulent and nonpathogenic P. syringae strains were modulated by salicylate as well as by ET and JA responses. This work underscores the complexity of plant immune responses to pathogens with distinct pathogenesis strategies, shows how BIK1 may be linked to promotion or suppression of disease, and provides insight to the complex interplay between plant growth and defense. Interestingly, although BIK1 shares high sequence similarity to many Arabidopsis receptor-like cytoplasmic kinases, its function in defense against necrotrophic infection and responses to ET appears to be unique.