Recognition of pathogen effectors is a crucial step for triggering plant immunity. Resistance (R) genes often encode for nucleotide-binding leucine-rich repeat receptors (NLRs), and NLRs detect ...effectors from pathogens to trigger effector-triggered immunity (ETI). NLR recognition of effectors is observed in diverse forms where NLRs directly interact with effectors or indirectly detect effectors by monitoring host guardees/decoys (HGDs). HGDs undergo different biochemical modifications by diverse effectors and expand the effector recognition spectrum of NLRs, contributing robustness to plant immunity. Interestingly, in many cases of the indirect recognition of effectors, HGD families targeted by effectors are conserved across the plant species while NLRs are not. Notably, a family of diversified HGDs can activate multiple non-orthologous NLRs across plant species. Further investigation on HGDs would reveal the mechanistic basis of how the diversification of HGDs confers novel effector recognition by NLRs.
Enhanced Disease Susceptibility1 (EDS1) is an important regulator of plant basal and receptor-triggered immunity. Arabidopsis EDS1 interacts with two related proteins, Phytoalexin Deficient4 (PAD4) ...and Senescence Associated Gene101 (SAG101), whose combined activities are essential for defense signaling. The different sizes and intracellular distributions of EDS1—PAD4 and EDS1—SAG101 complexes in Arabidopsis leaf tissues suggest that they perform nonredundant functions. The nature and biological relevance of EDS1 interactions with PAD4 and SAG101 were explored using yeast three-hybrid assays, in vitro analysis of recombinant proteins purified from Escherichia coli, and characterization of Arabidopsis transgenic plants expressing an eds1 mutant (eds1 L262P ) protein which no longer binds PAD4 but retains interaction with SAG101. EDS1 forms molecularly distinct complexes with PAD4 or SAG101 without additional plant factors. Loss of interaction with EDS1 reduces PAD4 post-transcriptional accumulation, consistent with the EDS1 physical association stabilizing PAD4. The dissociated forms of EDS1 and PAD4 are fully competent in signaling receptor-triggered localized cell death at infection foci. By contrast, an EDS1—PAD4 complex is necessary for basal resistance involving transcriptional up-regulation of PAD4 itself and mobilization of salicylic acid defenses. Different EDS1 and PAD4 molecular configurations have distinct and separable functions in the plant innate immune response.
Rosa chinensis is an important economic and ornamental crop, but powdery mildew greatly reduces its ornamental and economic value. The RcCPR5 gene, encoding a constitutive expressor of ...pathogenesis-related genes, has two splicing variants in R. chinensis. Compared with RcCPR5-1, RcCPR5-2 has a large C-terminal deletion. During disease development, RcCPR5-2 responded quickly and coordinated with RcCPR5-1 to resist the invasion of the powdery mildew pathogen. In virus-induced gene silencing experiments, down-regulation of RcCPR5 improved the resistance of R. chinensis to powdery mildew. This was confirmed to be broad-spectrum resistance. In the absence of pathogen infection, RcCPR5-1 and RcCPR5-2 formed homodimers and heterodimers to regulate plant growth; but when infected by the powdery mildew pathogen, the RcCPR5-1 and RcCPR5-2 complexes disassociated and released RcSIM/RcSMR to induce effector-triggered immunity, thereby inducing resistance to pathogen infection.
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•A major QTL for aflatoxin production resistance was identified in a 1.98 Mbp genomic region by both NGS-based QTL-seq approach and genetic linkage analysis.•A gene namely AhAftr1, ...annotated as “NB-LRRs protein gene” with structural variation (SV) in the LRRs domain between parental lines was identified by fine-mapping using a secondary segregation mapping population.•Transgenic experiments confirmed that the SV of AhAftr1 confers aflatoxin production resistance.•RNA-Seq and differential gene expression analysis indicated that AhAftr1 might be involved in disease resistance via the ETI pathway.•Thirty-six lines were identified from a special panel of germplasm accessions and breeding lines by using AFTR.Del.A07 , which was developed based on the SV, and their aflatoxin content were decreased by over 77.67% compared to the susceptible control Zhonghua12.
Peanut is susceptible to infection of Aspergillus fungi and conducive to aflatoxin contamination, hence developing aflatoxin-resistant variety is highly meaningful. Identifying functional genes or loci conferring aflatoxin resistance and molecular diagnostic marker are crucial for peanut breeding.
This work aims to (1) identify candidate gene for aflatoxin production resistance, (2) reveal the related resistance mechanism, and (3) develop diagnostic marker for resistance breeding program.
Resistance to aflatoxin production in a recombined inbred line (RIL) population derived from a high-yielding variety Xuhua13 crossed with an aflatoxin-resistant genotype Zhonghua 6 was evaluated under artificial inoculation for three consecutive years. Both genetic linkage analysis and QTL-seq were conducted for QTL mapping. The candidate gene was further fine-mapped using a secondary segregation mapping population and validated by transgenic experiments. RNA-Seq analysis among resistant and susceptible RILs was used to reveal the resistance pathway for the candidate genes.
The major effect QTL qAFTRA07.1 for aflatoxin production resistance was mapped to a 1.98 Mbp interval. A gene, AhAftr1 (Arachis hypogaea Aflatoxin resistance 1), was detected structure variation (SV) in leucine rich repeat (LRR) domain of its production, and involved in disease resistance response through the effector-triggered immunity (ETI) pathway. Transgenic plants with overexpression of AhAftr1(ZH6) exhibited 57.3% aflatoxin reduction compared to that of AhAftr1(XH13). A molecular diagnostic marker AFTR.Del.A07 was developed based on the SV. Thirty-six lines, with aflatoxin content decrease by over 77.67% compared to the susceptible control Zhonghua12 (ZH12), were identified from a panel of peanut germplasm accessions and breeding lines through using AFTR.Del.A07.
Our findings would provide insights of aflatoxin production resistance mechanisms and laid meaningful foundation for further breeding programs.
Fusarium oxysoporum f. sp. radicis‐cucumerinum (Forc) is able to cause disease in cucumber, melon, and watermelon, while F. oxysporum f. sp. melonis (Fom) can only infect melon plants. Earlier ...research showed that mobile chromosomes in Forc and Fom determine the difference in host range between Forc and Fom. By closely comparing these pathogenicity chromosomes combined with RNA‐sequencing data, we selected 11 candidate genes that we tested for involvement in the difference in host range between Forc and Fom. One of these candidates is a putative effector gene on the Fom pathogenicity chromosome that has nonidentical homologs on the Forc pathogenicity chromosome. Four independent Forc transformants with this gene from Fom showed strongly reduced or no pathogenicity towards cucumber, while retaining pathogenicity towards melon and watermelon. This suggests that the protein encoded by this gene is recognized by an immune receptor in cucumber plants. This is the first time that a single gene has been demonstrated to determine a difference in host specificity between formae speciales of F. oxysporum.
A single putative effector gene from melon‐infecting Fusarium oxysporum f. sp. melonis is able to turn cucumber‐, melon‐ and watermelon‐infecting F. oxysoporum f. sp. radicis‐cucumerinum nonpathogenic towards cucumber plants.
Plants can detect microbial molecules via surface-localized pattern-recognition receptors (PRRs) and intracellular immune receptors from the nucleotide-binding, leucine-rich repeat receptor (NLR) ...family. The corresponding pattern-triggered (PTI) and effector-triggered (ETI) immunity were long considered separate pathways, although they converge on largely similar cellular responses, such as calcium influx and overlapping gene reprogramming. A number of studies recently uncovered genetic and molecular interconnections between PTI and ETI, highlighting the complexity of the plant immune network. Notably, PRR- and NLR-mediated immune responses require and potentiate each other to reach an optimal immune output. How PTI and ETI connect to confer robust immunity in different plant species, including crops will be an exciting future research area.
•NLRs oligomerize upon activation to function as ion channels or enzymes.•PRRs and NLRs converge on common immune responses, including direct Ca2+ influx.•PRR and NLR immunity share genetic requirements and potentiate each other.•Immune receptor networks and connections evolve differently in plant species.
Plants respond to
infestation through two layers of immune system (PTI and ETI). This process involves the production of plant-induced resistance. Strategies for inducing resistance in plants include ...the formation of tyloses, gels, and callose and changes in the content of cell wall components such as cellulose, hemicellulose, pectin, lignin, and suberin in response to pathogen infestation. When
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secrete cell wall degrading enzymes, plants also sense the status of cell wall fragments through the cell wall integrity (CWI) system, which activates deep-seated defense responses. In addition, plants also fight against
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infestation by regulating the distribution of metabolic networks to increase the production of resistant metabolites and reduce the production of metabolites that are easily exploited by
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. We review the strategies used by plants to induce resistance in response to
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infestation. In particular, we highlight the importance of plant-induced physical and chemical defenses as well as cell wall defenses in the fight against
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