Shweta Chhajed

Systemic acquired resistance (SAR) is a long-lasting broad-spectrum plant defense mechanism induced in distal systemic tissues by mobile signals generated at the primary infection site. Despite the discoveries of multiple potential mobile signals, how these signals cooperate to trigger downstream SAR signaling is unknown. Here, we show that endogenous extracellular nicotinamide adenine dinucleotide (phosphate) [eNAD(P)] accumulates systemically upon pathogen infection and that both eNAD(P) and the lectin receptor kinase (LecRK), LecRK-VI.2, are required in systemic tissues for the establishment of SAR. Moreover, putative mobile signals, e.g., N-hydroxypipecolic acid (NHP), trigger de novo systemic eNAD(P) accumulation largely through the respiratory burst oxidase homolog RBOHF-produced reactive oxygen species (ROS). Importantly, NHP-induced systemic immunity mainly depends on ROS, eNAD(P), LecRK-VI.2, and BAK1, indicating that NHP induces SAR primarily through the ROS-eNAD(P)-LecRK-VI.2/BAK1 signaling pathway. Our results suggest that mobile signals converge on eNAD(P) in systemic tissues to trigger SAR through LecRK-VI.2.

Phosphorylation can quickly switch on/off protein functions. Here, we reported pre-mRNA processing 4 kinase A (PRP4KA), and its paralogs interact with Serrate (SE), a key factor in RNA processing. PRP4KA phosphorylates at least five residues of SE in vitro and in vivo. Hypophosphorylated, but not hyperphosphorylated, SE variants could readily rescue se phenotypes in vivo. Moreover, hypophosphorylated SE variants had stronger binding affinity to microprocessor component HYL1 and were more resistant to degradation by 20 S proteasome than hyperphosphorylated counterparts. Knockdown of the kinases enhanced the accumulation of hypophosphorylated SE. However, the excessive SE interfered with the assembly and function of SE-scaffolded macromolecule complexes, causing the se -like defects in the mutant and wild-type backgrounds. Thus, phosphorylation of SE via PRP4KA can quickly clear accumulated SE to secure its proper amount. This study provides new insight into how protein phosphorylation regulates miRNA metabolism through controlling homeostasis of SE accumulation in plants.

Insect pests represent a major global challenge to important agricultural crops. Insecticides are often applied to combat such pests, but their use has caused additional challenges such as environmental contamination and human health issues. Over millions of years, plants have evolved natural defense mechanisms to overcome insect pests and pathogens. One such mechanism is the production of natural repellents or specialized metabolites like glucosinolates. There are three types of glucosinolates produced in the order Brassicales: aliphatic, indole, and benzenic glucosinolates. Upon insect herbivory, a “mustard oil bomb” consisting of glucosinolates and their hydrolyzing enzymes (myrosinases) is triggered to release toxic degradation products that act as insect deterrents. This review aims to provide a comprehensive summary of glucosinolate biosynthesis, the “mustard oil bomb”, and how these metabolites function in plant defense against pathogens and insects. Understanding these defense mechanisms will not only allow us to harness the benefits of this group of natural metabolites for enhancing pest control in Brassicales crops but also to transfer the “mustard oil bomb” to non-glucosinolate producing crops to boost their defense and thereby reduce the use of chemical pesticides.

Early age-related developmental senescence was observed in Arabidopsis cyp79B2/cyp79B3 double mutants that cannot produce indole-3-acetaldoxime (IAOx), the precursor to indole glucosinolates (IGs), camalexin and auxin. The early senescence phenotype was not observed when senescence was induced by darkness. The cyp79B2/cyp79B3 mutants had lower auxin levels, but did not display auxin-deficient phenotypes. Camalexin biosynthesis mutants senesced normally; however, IG-transport and exosome-related pen1/pen3 double mutants displayed early senescence. The early senescence in pen1/pen3 mutants depended on salicylic acid and was not observed in pen1 or pen3 single mutants. Quantitation of IGs showed reduced levels in cyp79B2/cyp79B3 mutants, but unchanged levels in pen1/pen3, even though both of these double mutants display early senescence. We discuss how these genetic data provide evidence that IAOx metabolite(s) are playing a protective role in leaf senescence that is dependent on proper trafficking by PEN1 and PEN3, perhaps via the formation of exosomes.

Combining genetic engineering of MPK4 activity and quantitative proteomics, we established an in planta system that enables rapid study of MPK4 signaling n

To determine how the dormancy-breaking agent hydrogen cyanamide (HC) advances budbreak in peach ( Prunus persica ), this study compared the transcriptome of buds of low-chill ‘TropicBeauty’ peach trees treated with 1% (v/v) HC and that of nontreated trees at 3 and 7 days after treatment (DAT), respectively, using an RNA sequencing analysis. The peak of total budbreak occurred 6 weeks earlier in the HC-treated trees (at 32 DAT) than the nontreated trees (at 74 DAT). There were 1312 and 1095 differentially expressed genes (DEGs) at 3 and 7 DAT, respectively. At 3 DAT, DEGs related to oxidative stress, including the response to hypoxia, lipid oxidation, and reactive oxygen species (ROS) metabolic process, were upregulated in HC-treated buds. Additionally, DEGs encoding enzymes for ROS scavenging and the pentose phosphate pathway were upregulated at 3 DAT but they were not differently expressed at 7 DAT, indicating a temporary demand for defense mechanisms against HC-triggered oxidative stress. Upregulation of DEGs for cell division and development at 7 DAT, which were downregulated at 3 DAT, suggests that cell activity was initially suppressed but was enhanced within 7 DAT. At 7 DAT, DEGs related to cell wall degradation and modification were upregulated, which was possibly responsible for the burst of buds. The results of this study strongly suggest that HC induces transient oxidative stress shortly after application, leading to the release of bud dormancy and, subsequently, causing an increase in cell activity and cell wall loosening, thereby accelerating budbreak in peach.

Glucosinolates (GLSs) are a well-defined group of specialized metabolites, and like any other plant specialized metabolites their presence does not directly affect the plant survival in terms of growth and development. However, specialized metabolites are essential to combat environmental stresses, such as pathogens and herbivores. GLSs naturally occur in many pungent plants in the order of Brassicales. To date, more than 200 different GLS structures have been characterized and their distribution differs from species to species. GLSs co-exist with classical and atypical myrosinases, which can hydrolyze GLS into an unstable aglycone thiohydroximate-O-sulfonate, which rearranges to produce different degradation products. GLSs, myrosinases, myrosinase interacting proteins, and GLS degradation products constitute the GLS-myrosinase (GM) system (‘mustard oil bomb’). This review discusses the cellular and subcellular organization of the GM system, its chemodiversity, and functions in different cell-types. Although there are many studies on the functions of GLSs and/or myrosinases at the tissue and whole plant levels, very few studies have focused on different single cell-types. Single cell-type studies will help to reveal specific functions that are missed at the tissue and organismal level. This review aims to highlight: (a) recent progress in cellular and subcellular compartmentation of GLSs, myrosinases, and myrosinase interacting proteins; (b) molecular and biochemical diversity of GLSs and myrosinases; and (c) myrosinase interaction with its interacting proteins, and how it regulates the degradation of GLSs and thus the biological functions (e.g., plant defense against pathogens). Future prospects may include targeted approaches for engineering/breeding of plants and crops in the cell-type specific manner towards enhanced plant defense and nutrition.

For field-grown ‘Valencia’ sweet orange ( Citrus sinensis ) affected by Huanglongbing [HLB ( Candidatus Liberibacter asiaticus ( C Las)], trees that displayed more severe HLB symptoms (severe trees) had 74% fruit drop before harvest; however, the drop rate for less symptomatic trees (mild trees) was 45%. For mature fruit (3 weeks before harvest) still attached to the branches, 60% of them from severe trees were “loose fruit” [fruit detachment force (FT) < 6 kgf]. In contrast, only 13% of the attached fruit from the mild trees were loose. Overall, fresh weight and size of loose fruit were lower than “tight fruit” (FT > 6 kgf). Irrespective of the symptom levels of trees, the concentrations of glucose, fructose, and inositol in juice of loose fruit were the same or larger than those of tight fruit, suggesting that the shortage of carbohydrates is not the dominant cause of HLB-associated preharvest fruit drop. Expression levels of the cell wall modification genes encoding cellulase (endo-1,4-β-glucanase), polygalacturonase, and pectate lyase were greater in the calyx abscission zones of loose fruit compared to tight fruit, indicating that cell separation was occurring in the former at the time of collection. No differences in the expression levels of genes encoding the ethylene biosynthesis enzymes, including 1-aminocyclopropane-1-carboxylic acid (ACC) synthase ( ACS ) and ACC oxidase ( ACO ), and an ethylene-responsive transcription factor 1 ( ERF1 ) were observed in tissues of loose and tight fruit. Interestingly, ACS , ACO , and EFR1 expressions were lower in calyx abscission zones and in leaves of the severe trees compared with those of mild trees, suggesting an ostensible, HLB-dependent reduction in ethylene biosynthesis and/or signaling close to harvest time. However, the role of ethylene in HLB-associated preharvest fruit drop remains to be determined. The results leave open the possibility of early ethylene production and action before the initiation of fruit abscission.