Search

Fatty acids (FA) and lipids are well known regulators of plant defense. Our previous studies have shown that components of prokaryotic (plastidal) FA biosynthesis pathway regulate various aspects of plant defense. Here, we investigated the defense related roles of the soluble acyl CoA binding proteins (ACBPs), which are thought to facilitate the intracellular transport of FA/lipids. We show that ACBP3 and 4 are required for maintaining normal lipid levels and that ACBP3 contributes to the lipid flux between the prokaryotic and eukaryotic pathways. We also show that loss of ACBP3, 4, or 6 impair normal development of the cuticle and affect both basal and resistance protein-mediated defense against bacterial and fungal pathogens. Loss of ACBP3, 4, or 6 also inhibits the induction of systemic acquired resistance (SAR) due to the plants inability to generate SAR inducing signal(s). Together, these data show that ACBP3, ACBP4, and ACBP6 are required for cuticle development as well as defense against microbial pathogens. [ABSTRACT FROM AUTHOR]

Systemic acquired resistance (SAR) is a form of defense that provides resistance against a broad spectrum of pathogens in plants. Previous work indicates a role for plastidial glycerolipid biosynthesis in SAR. Specifically, mutations in FATTY ACID DESATURASE7 (FAD7), which lead to reduced trienoic fatty acid levels and compromised plastidial lipid biosynthesis, have been associated with defective SAR. We show that the defective SAR in Arabidopsis (Arabidopsis thaliana)fad7-1 plants is not associated with a mutation in FAD7 but rather with a second-site mutation in GLABRA1 (GL1), a gene well known for its role in trichome formation. The compromised SAR in gll plants is associated with impairment in their cuticles. Furthermore, mutations in two other components of trichome development, GL3 and TRANSPARENT TESTA GLABRA1, also impaired cuticle development and SAR. This suggests an overlap in the biochemical pathways leading to cuticle and trichome development. Interestingly, exogenous application of gibberellic acid (GA) not only enhanced SAR in wild-type plants but also restored SAR in gl1 plants. In contrast to GA, the defense phytohoromes salicylic acid and jasmonic acid were unable to restore SAR in gl1 plants. GA application increased levels of cuticular components but not trichome formation on gl1 plants, thus implicating cuticle, but not trichomes, as an important component of SAR. Our findings question the prudence of using mutant backgrounds for genetic screens and underscore a need to reevaluate phenotypes previously studied in the gl1 background. [ABSTRACT FROM AUTHOR]

Light harvested by plants is essential for the survival of most life forms. This light perception ability requires the activities of proteins termed photoreceptors. We report a function for photoreceptors in mediating resistance (R) protein-derived plant defense. The bluelight photoreceptors. cryptochrome (CRY) 2 and phototropin (PHOT) 2. are required for the stability of the R protein HRT, and thereby resistance to Turnip Crinkle virus (TCV). Exposure to darkness or blue-light induces degradation of CRY2, and in turn HRT. resulting in susceptibility. Overexpression of HRT can compensate for the absence of PHOT2 but not CRY2. HRT does not directly associate with either CRY2 or PHOT2 but does bind the CRY2-/PHOT2-interacting E3 ubiquitin ligase, COP1. Application of the proteasome inhibitor, MGi 32, prevents blue-light-dependent degradation of HRT. consequently these plants show resistance to TCV under blue-light. We propose that CRY2/PHOT2 negatively regulate the proteasomemediated degradation of HRT, likely via COPt and blue-light relieves this repression resutting in HRT degradation. [ABSTRACT FROM AUTHOR]

Inoculation of turnip crinkle virus (TCV) on the resistantArabidopsisecotype Di-17 elicits a hypersensitive response (HR), which is accompanied by increased expression of pathogenesis-related (PR) genes. Previous genetic analyses revealed that the HR to TCV is conferred byHRT, which encodes a coiled-coil (CC), nucleotide-binding site (NBS) and leucine-rich repeat (LRR) class resistance (R) protein. In contrast to the HR, resistance to TCV requires bothHRTand a recessive allele at a second locus designatedrrt. Here, we demonstrate that unlike most CC-NBS-LRRRgenes,HRT/rrt-mediated resistance is dependent onEDS1and independent ofNDR1. Resistance is also independent ofRAR1andSGT1.HRT/rrt-mediated resistance is compromised in plants with reduced salicylic acid (SA) content as a consequence of mutationseds5,pad4, orsid2.By contrast, HR is not affected by mutations ineds1,eds5,pad4,sid2,ndr1,rar1, orsgt1b.Resistance to TCV is restored in both SA-deficient Di-17 plants expressing thenahGtransgene and mutants containing theeds1,eds5, orsid2mutations by exogenous application of SA or the SA analog benzo(1,2,3)thiadiazole-7-carbothioic acid (BTH). In contrast, SA/BTH treatment failed to enhance resistance inHRT pad4, Col-0, orhrthomozygous progeny of a cross between Di-17 and Col-0. Thus, HRT and PAD4 are required for SA-induced resistance. Exogenously supplied SA or high endogenous levels of SA, due to thessi2mutation, overcame the suppressive effects ofRRTand enhanced resistance to TCV, provided theHRTallele was present. High levels of SA upregulateHRTexpression via aPAD4-dependent pathway. As Col-0 transgenic lines expressing high levels ofHRTwere resistant to TCV, but lines expressing moderate to low levels ofHRTwere not, we conclude that SA enhances resistance in theRRTbackground by upregulatingHRTexpression. These data suggest that the HRT-TCV interaction is unable to generate sufficient amounts of SA required for a stable resistance phenotype, and the presence ofrrtpossibly corrects this deficiency. [ABSTRACT FROM AUTHOR]

The article discusses plant cuticle regulates apoplastic transport of salicylic acid during systemic acquired resistance. It mentions that increased transpiration and reduced water potential preferentially routes Salicylic Acid (SA) to cuticle wax rather than to the apoplast in cuticle-defective mutants. It also mentions that cuticle impairment reduces water potential and, thereby, apoplastic transport of SA.

Summary: Epigenetic modifications have emerged as an important mechanism underlying plant defence against pathogens. We examined the role of JMJ14, a Jumonji (JMJ) domain‐containing H3K4 demethylase, in local and systemic plant immune responses in Arabidopsis.The function of JMJ14 in local or systemic defence response was investigated by pathogen growth assays and by analysing expression and H3K4me3 enrichments of key defence genes using qPCR and ChIP‐qPCR. Salicylic acid (SA) and pipecolic acid (Pip) levels were quantified and function of JMJ14 in SA‐ and Pip‐mediated defences was analysed in Col‐0 and jmj14 plants.jmj14 mutants were compromised in both local and systemic defences. JMJ14 positively regulates pathogen‐induced H3K4me3 enrichment and expression of defence genes involved in SA‐ and Pip‐mediated defence pathways. Consequently, loss of JMJ14 results in attenuated defence gene expression and reduced Pip accumulation during establishment of systemic acquired resistance (SAR). Exogenous Pip partially restored SAR in jmj14 plants, suggesting that JMJ14 regulated Pip biosynthesis and other downstream factors regulate SAR in jmj14 plants.JMJ14 positively modulates defence gene expressions and Pip levels in Arabidopsis. [ABSTRACT FROM AUTHOR]

The article offers information on Pipecolic acid (Pip), a non-proteinaceous product of lysine catabolism, which is an important regulator of immunity in plants and human beings. It mentions that Pip accumulates on pathogen infection in plants and has been related to systemic acquired resistance (SAR).

With the legalization of industrial hemp in the United States, defined based on tetrahydrocannabinol (THC) dry weight content of ≤ 0.3%, the market for various cannabinoids including cannabidiol (CBD), cannabinol (CBN), cannabigerol (CBG), and cannabichromene (CBC) have flourished. The current measurement methods such as ultra-high performance liquid chromatography and gas chromatography (GC) require sophisticated instruments and trained personnel and are time-consuming. Therefore, there is a critical need for a rapid and reliable method to measure cannabinoids for regulatory compliance, determination of usage, and for quality control. Here, we report the use of near-infrared spectroscopy (NIRS) for rapid measurement of moisture content (MC) and cannabinoid contents of ground and whole hemp and rapid identification of legal from illegal industrial hemp. Good NIRS quantitative predictions were obtained for MC of ground and whole hemp, THC of ground hemp, CBD of ground and whole hemp, and CBC of whole hemp. Binary classification of industrial hemp as legal (≤0.3% THC) or illegal was performed using discriminant analysis and thresholding models. Discriminant calibration models developed showed correct classifications (CC) ranging from 93.0% to 94.0% with CC for independent validation at 83.9–87.5%. The concurrent multi-constituent predictions of MC and THC using NIRS allows for real-time adjustments of cannabinoid contents and rapid identification of legal or illegal hemp. These are important tools that will benefit the hemp industry, regulators, farmers, and consumers. [Display omitted] • NIR spectroscopy can measure moisture content (MC) and various cannabinoids of whole and ground hemp. • NIR-predicted MCs of whole and ground hemp are accurate (R2 of 0.91 and 0.94 and SEPs of 1.28 and 1.24). • Good NIRS quantitative predictions were obtained for THC of ground hemp, CBD of ground and whole hemp, and CBC of whole hemp. • NIR-based identification of legal versus illegal hemp through discriminant analysis showed correct classification of up to 87.5%. [ABSTRACT FROM AUTHOR]

Eukaryotic elongation factors (eEFs) are protein factors that mediate the extension of peptide chain, among which eukaryotic elongation factor 1 alpha (eEF1A) is one of the most abundant protein synthesis factors. Previously we showed that the P3 protein of Soybean mosaic virus (SMV), one of the most destructive and successful viral pathogens of soybean, targets a component of the soybean translation elongation complex to facilitate its pathogenesis. Here, we conducted a systematic analyses of the soybean eEF ( GmeEF ) gene family in soybean and examinedits role in virus resistance. In this study, GmeEF family members were identified and characterized based on sequence analysis. The 42 members, which were unevenly distributed across the 15 chromosomes, were renamed according to their chromosomal locations. The GmeEF members were further divided into 12 subgroups based on conserved motif, gene structure, and phylogenetic analyses. Analysis of the promoter regions showed conspicuous presence of myelocytomatosis (MYC) and ethylene-responsive (ERE) cis-acting elements, which are typically involved in drought and phytohormone response, respectively, and thereby in plant stress response signaling. Transcriptome data showed that the expression of 15 GmeEF gene family members changed significantly in response to SMV infection. To further examine EF1A function in pathogen response, three different Arabidopsis mutants carrying T-DNA insertions in orthologous genes were analyzed for their response to Turnip crinkle virus (TCV) and Cucumber mosaic virus (CMV). Results showed that there was no difference in viral response between the mutants and the wild type plants. This study provides a systematic analysis of the GmeEF gene family through analysis of expression patterns and predicted protein features. Our results lay a foundation for understanding the role of eEF gene in soybean anti-viral response., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Luan, Song, Huang, Li, Xu, Kachroo, Kachroo and Zhao.)

Plants possess a unique form of broad-spectrum long-distance immunity termed systemic acquired resistance (SAR). SAR involves the rapid generation of mobile signal(s) in response to localized microbial infection, which transport to the distal tissue and 'prime' them against future infections by related and unrelated pathogens. Several SAR-inducing chemicals that could be classified as the potential mobile signal have been identified. Many of these function in a bifurcate pathway with both branches being equally essential for SAR induction. This review reflects on the potential candidacy of the known SAR inducers as mobile signal(s) based on historical knowledge of the SAR signal and recent advances in the SAR signaling pathway., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Loss of a stearoyl-ACP desaturase activity in the Arabidopsis thaliana ssi2 mutant confers susceptibility to the necrotroph, Botrytis cinerea. In contrast, the ssi2 mutant exhibits enhanced resistance to Pseudomonas syringae, Peronospora parasitica, and Cucumber mosaic virus. The altered basal resistance to these pathogens in the ssi2 mutant plant is accompanied by the constitutive accumulation of elevated salicylic acid (SA) level and expression of the pathogenesis-related 1 (PR1) gene, the inability of jasmonic acid (JA) to activate expression of the defensin gene, PDF1.2, and the spontaneous death of cells. Here, we show that presence of the eds5 and pad4 mutant alleles compromises the ssi2-conferred resistance to Pseudomonas syringae pv. maculicola. In contrast, resistance to B. cinerea was restored in the ssi2 eds5 and ssi2 pad4 double-mutant plants. However, resistance to B. cinerea was not accompanied by the restoration of JA responsiveness in the ssi2 eds5 and ssi2 pad4 plants. The ssi2 eds5 and ssi2 pad4 plants retain the ssi2-conferred spontaneous cell death phenotype, suggesting that cell death is not a major factor that predisposes the ssi2 mutant to infection by B. cinerea. Furthermore, the high SA content of the ssi2 pad4 plant, combined with our previous observation that the SA-deficient ssi2 nahG plant succumbs to infection by B. cinerea, suggests that elevated SA level does not have a causal role in the ssi2-conferred susceptibility to B. cinerea. Our results suggest that interaction between an SSI2-dependent factor or factors and an EDS5- and PAD4-dependent mechanism or mechanisms modulates defense to B. cinerea.