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ABSTRACT Necrotrophic pathogens cause serious threats to agricultural crops, and understanding the resistance genes and their genetic networks is key to breeding new plant cultivars with better resistance traits. AlthoughAlternaria alternatacauses black spot in important leafy brassica vegetables, and leads to significant loss of yield and food quality, little is known about plant–A. alternatainteractions. In this study, we used a unique and large collection of single, double and triple mutant lines of defence metabolite regulators inArabidopsisto explore how these transcription factors and their epistatic networks may influenceA. alternatainfections. This identified nine novel regulators and 20 pairs of epistatic interactions that modulateArabidopsisplants' defence responses toA. alternatainfection. We further showed that the glucosinolate 4‐methoxy‐indol‐3‐ylmethyl is the only glucosinolate consistently responsive toA. alternatainfection in Col‐0 ecotype. With the further exploration of the regulators and the genetic networks on modulating the accumulation of glucosinolates underA. alternatainfection, an inverted triangle regulatory model was proposed forArabidopsisplants' defence responses at a metabolic level and a phenotypic level. 

Abstract The rhizosphere microbiome influences many aspects of plant fitness, including production of secondary compounds and defence against insect herbivores. Plants also modulate the composition of the microbial community in the rhizosphere via secretion of root exudates. We tested both the effect of the rhizosphere microbiome on plant traits, and host plant effects on rhizosphere microbes using recombinant inbred lines (RILs) ofBrassica rapathat differ in production of glucosinolates (GLS), secondary metabolites that contribute to defence against insect herbivores. First, we investigated the effect of genetic variation in GLS production on the composition of the rhizosphere microbiome. Using a Bayesian Dirichlet‐multinomial regression model (DMBVS), we identified both negative and positive associations between bacteria from six genera and the concentration of five GLS compounds produced in plant roots. Additionally, we tested the effects of microbial inoculation (an intact vs. disrupted soil microbiome) on GLS production and insect damage in these RILs. We found a significant microbial treatment × genotype interaction, in which total GLS was higher in the intact relative to the disrupted microbiome treatment in some RILs. However, despite differences in GLS production between microbial treatments, we observed no difference in insect damage between treatments. Together, these results provide evidence for a full feedback cycle of plant–microbe interactions mediated by GLS; that is, GLS compounds produced by the host plant “feed‐down” to influence rhizosphere microbial community and rhizosphere microbes “feed‐up” to influence GLS production. 

SUMMARY Meristem function is underpinned by numerous genes that affect hormone levels, ultimately controlling phyllotaxy, the transition to flowering and general growth properties. Class I KNOX genes are major contributors to this process, promoting cytokinin biosynthesis but repressing gibberellin production to condition a replication competent state. We identified a suppressor mutant of theKNOX1mutantbrevipedicellus(bp) that we termedflasher(fsh), which promotes stem and pedicel elongation, suppresses early senescence, and negatively affects reproductive development. Map‐based cloning and complementation tests revealed thatfshis due to an E40K change in the flavin monooxygenaseGS‐OX5, a gene encoding a glucosinolate (GSL) modifying enzyme.In vitroenzymatic assays revealed thatfshpoorly converts substrate to product, yet the levels of several GSLs are higher in the suppressor line, implicatingFSHin feedback control of GSL flux.FSHis expressed predominantly in the vasculature in patterns that do not significantly overlap those ofBP, implying a non‐cell autonomous mode of meristem control via one or more GSL metabolites. Hormone analyses revealed that cytokinin levels are low inbp, butfshrestores cytokinin levels to near normal by activating cytokinin biosynthesis genes. In addition, jasmonate levels in thefshsuppressor are significantly lower than inbp, which is likely due to elevated expression of JA inactivating genes. These observations suggest the involvement of the GSL pathway in generating one or more negative effectors of growth that influence inflorescence architecture and fecundity by altering the balance of hormonal regulators.