Search

SUMMARY Plants recognize molecules related to a variety of biotic stresses through pattern recognition receptors to activate plant immunity. In the interactions between plants and chewing herbivores, such as lepidopteran larvae, oral secretions (OS) are deposited on wounded sites, which results in the elicitation of plant immune responses. The widely conserved receptor‐like kinase CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1) has been broadly associated with the recognition of microbial components, such as fungal chitin, but its relevance to herbivory remained unclear. In this study, we used receptor‐knockout rice (Oryza sativa) and larvae of the lepidopteran pest Mythimna loreyi to demonstrate that the induction of immune responses triggered by larval OS in rice cells largely depends on CERK1 (OsCERK1). CHITIN ELICITOR‐BINDING PROTEIN (CEBiP), an OsCERK1‐interacting receptor‐like protein that was proposed as the main chitin receptor, also contributed to the responses of rice cells to OS collected from three different lepidopteran species. Furthermore, CEBiP knockout rice seedlings showed lower OS‐triggered accumulation of jasmonic acid. These results strongly suggest that the OsCERK1 and CEBiP recognize a particular OS component in chewing lepidopteran herbivores, and point toward the presence of chitooligosaccharides in the OS. Targeted perturbation to chitin recognition, through the use of fungal effector proteins, confirmed the presence of chitooligosaccharides in the OS. Treatments of wounds on rice plants with chitooligosaccharides enhanced a set of immune responses, leading to resistance against an herbivorous insect. Our data show that rice recognizes chitooligosaccharides during larval herbivory to activate resistance, and identifies chitin as a novel herbivore‐associated molecular pattern. [ABSTRACT FROM AUTHOR]

The dasABC genes encode an ATP-binding cassette (ABC) transporter, which is one of the uptake systems for N,N'-diacetylchitobiose [[(GIcNAc).sub.2]] in Streptomyces coelicolor A3(2), although the gene encoding the ABC subunit that provides ATP hydrolysis for DasABC has not been identified. In this study, we disrupted the sequence that is highly homologous to the msiK gene, the product of which is an ABC subunit assisting several ABC permeases in other Streptomyces species. Disruption of msiK severely affected the ability of S. coeficolor A3(2) to utilize maltose, cellobiose, starch, cellulose, chitin and chitosan, but not glucose. The msiK null mutant lacked [(GIcNAc).sub.2]-uptake activity, but GIcNAc transport activity was unaffected. The data indicated that msiK is essential for [(GIcNAc).sub.2] uptake, which in S. coelicolor A3(2) is governed by ABC transporters including the DasABC-MsiK system, in contrast to Escherichia coil and Serratia marcescens, in which [(GIcNAc).sub.2] uptake is mediated by the phosphotransferase system. Interestingly, the induction of chitinase production by [(GIcNAc).sub.2] or chitin was absent in the msiK null mutant, unlike in the parent strain M145. The defect in chitinase gene induction was rescued by expressing the His-tagged MsiK protein under the control of the putative native promoter on a multicopy plasmid. The data suggest that uptake of [(GIcNAc).sub.2] is necessary for induction of chitinase production. The msiK gene was constitutively transcribed, whereas the transcription of dasA [[(GIcNAc).sub.2]-binding protein gene], malE (putative maltose-binding protein gene), cebE1 (putative cellobiose-binding protein gene) and bxlE1 (putative xylobiose-binding protein gene) was induced by their corresponding sugar ligands. This is believed to be the first report to indicate that [(GIcNAc).sub.2] uptake mediated by ABC transporters is essential for chitinase production in streptomycetes, which are known to be the main degraders of chitin in soil.

The transporter genes for N,N'-diacetylchitobiose [(GlcNAc).sub.2] in the genome of Streptomyces coelicolor A3(2) was explored by the direct repeat sequence as a probe to determine the [(GlcNAc).sub.2] uptake activity which was induced by the amino sugar itself.

Success of plants largely depends on their ability to defend against herbivores. Since emergence of the first voracious consumers, plants maintained adapting their structures and chemistry to escape from extinction. The constant pressure was further accelerated by adaptation of herbivores to plant defenses, which all together sparked the rise of a chemical empire comprised of thousands of specialized metabolites currently found in plants. Metabolic diversity in the plant kingdom is truly amazing, and although many plant metabolites have already been identified, a large number of potentially useful chemicals remain unexplored in plant bio‐resources. Similarly, biosynthetic routes for plant metabolites involve many enzymes, some of which still wait for identification and biochemical characterization. Moreover, regulatory mechanisms that control gene expression and enzyme activities in specialized metabolism of plants are scarcely known. Finally, understanding of how plant defense chemicals exert their toxicity and/or repellency against herbivores remains limited to typical examples, such as proteinase inhibitors, cyanogenic compounds and nicotine. In this review, we attempt summarizing the current status quo in metabolic defense of plants that is predominantly based on the survey of ubiquitous examples of plant interactions with chewing herbivores. [ABSTRACT FROM AUTHOR]