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Summary: The Gy14 cucumber (Cucumis sativus) is resistant to oomyceteous downy mildew (DM), bacterial angular leaf spot (ALS) and fungal anthracnose (AR) pathogens, but the underlying molecular mechanisms are unknown.Quantitative trait locus (QTL) mapping for the disease resistances in Gy14 and further map‐based cloning identified a candidate gene for the resistant loci, which was validated and functionally characterized by spatial‐temporal gene expression profiling, allelic diversity and phylogenetic analysis, as well as local association studies.We showed that the triple‐disease resistances in Gy14 were controlled by the cucumber STAYGREEN (CsSGR) gene. A single nucleotide polymorphism (SNP) in the coding region resulted in a nonsynonymous amino acid substitution in the CsSGR protein, and thus disease resistance. Genes in the chlorophyll degradation pathway showed differential expression between resistant and susceptible lines in response to pathogen inoculation. The causal SNP was significantly associated with disease resistances in natural and breeding populations. The resistance allele has undergone selection in cucumber breeding.The durable, broad‐spectrum disease resistance is caused by a loss‐of‐susceptibility mutation of CsSGR. Probably, this is achieved through the inhibition of reactive oxygen species over‐accumulation and phytotoxic catabolite over‐buildup in the chlorophyll degradation pathway. The CsSGR‐mediated host resistance represents a novel function of this highly conserved gene in plants. [ABSTRACT FROM AUTHOR]

Summary: Resistance against pathogens and herbivorous insects in many plant results from the expression of resistance (R) genes. Few reports, however, have considered the effects of elevated CO2 on R gene‐based resistance in plants. The current study determined the responses of two near isogenic Medicago truncatula genotypes (Jester has an R gene and A17 does not) to the pea aphid and elevated CO2 in open‐top chambers in the field. Aphid abundance, mean relative growth rate and feeding efficiency were increased by elevated CO2 on A17 plants but were reduced on Jester plants. According to proteomic and gene expression data, elevated CO2 enhanced pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI) but decreased the effector‐triggered immunity (ETI) in aphid‐infested A17 plants. For aphid‐infested Jester plants, by contrast, elevated CO2 enhanced the ETI‐related heat shock protein (HSP) 90 and its co‐chaperones, the jasmonic acid (JA) signaling pathway, and ubiquitin‐mediated proteolysis. In a loss‐of‐function experiment, silencing of the HSP90 gene in Jester plants impaired the JA signaling pathway and ubiquitin‐mediated proteolysis against the aphid under ambient CO2, and negated the increased resistance against the aphid under elevated CO2. Our results suggest that increases in expression of HSP90 are responsible for the enhanced resistance against the aphid under elevated CO2. [ABSTRACT FROM AUTHOR]

Candidate effectors from lettuce downy mildew ( Bremia lactucae) enable high-throughput germplasm screening for the presence of resistance ( R) genes. The nonhost species Lactuca saligna comprises a source of B. lactucae R genes that has hardly been exploited in lettuce breeding. Its cross-compatibility with the host species L. sativa enables the study of inheritance of nonhost resistance ( NHR)., We performed transient expression of candidate RXLR effector genes from B. lactucae in a diverse Lactuca germplasm set. Responses to two candidate effectors ( BLR31 and BLN08) were genetically mapped and tested for co-segregation with disease resistance., BLN08 induced a hypersensitive response (HR) in 55% of the L. saligna accessions, but responsiveness did not co-segregate with resistance to Bl:24. BLR31 triggered an HR in 5% of the L. saligna accessions, and revealed a novel R gene providing complete B. lactucae race Bl:24 resistance. Resistant hybrid plants that were BLR31 nonresponsive indicated other unlinked R genes and/or nonhost QTLs., We have identified a candidate avirulence effector of B. lactucae ( BLR31) and its cognate R gene in L. saligna. Concurrently, our results suggest that R genes are not required for NHR of L. saligna. [ABSTRACT FROM AUTHOR]

Xanthomonas transcription activator-like (TAL) effectors promote disease in plants by binding to and activating host susceptibility genes. Plants counter with TAL effector-activated executor resistance genes, which cause host cell death and block disease progression. We asked whether the functional specificity of an executor gene could be broadened by adding different TAL effector binding elements (EBEs) to it., We added six EBEs to the rice Xa27 gene, which confers resistance to strains of the bacterial blight pathogen Xanthomonas oryzae pv. oryzae ( Xoo) that deliver the TAL effector AvrXa27. The EBEs correspond to three other effectors from Xoo strain PXO99A and three from strain BLS256 of the bacterial leaf streak pathogen Xanthomonas oryzae pv. oryzicola ( Xoc)., Stable integration into rice produced healthy lines exhibiting gene activation by each TAL effector, and resistance to PXO99A, a PXO99A derivative lacking AvrXa27, and BLS256, as well as two other Xoo and 10 Xoc strains virulent toward wildtype Xa27 plants. Transcripts initiated primarily at a common site. Sequences in the EBEs were found to occur nonrandomly in rice promoters, suggesting an overlap with endogenous regulatory sequences., Thus, executor gene specificity can be broadened by adding EBEs, but caution is warranted because of the possible coincident introduction of endogenous regulatory elements. [ABSTRACT FROM AUTHOR]

• Host resistance to aphids is poorly understood. Medicago truncatula, a model legume and cultivated pasture species, was used to elucidate defense against two aphid species, Therioaphis trifolii f. maculata (spotted alfalfa aphid, SAA) and Acyrthosiphon kondoi (bluegreen aphid, BGA). • Aphid performance and plant damage were compared between near-isogenic cultivars, Mogul and Borung, that differ in resistance to both aphids. Analyses of aphid resistance in Mogul × Borung F2 plants and their progeny revealed modes of action and chromosome locations of resistance genes. • Separate genes were identified for SAA resistance ( TTR) and BGA resistance ( AKR); both mapped to chromosome 3 but were found to act independently to reduce survival and growth of their target aphid species. The TTR locus controls distinct, and contrasting, local and systemic plant responses between the near-isogenic cultivars. • TTR-mediated plant responses imply interaction between a resistance factor(s) in vascular tissue and a bioactive component(s) of SAA saliva. Features of both resistance traits suggest homology to aphid resistance in other legumes; elucidation of their molecular mechanisms will likely apply to other aphid–plant interactions. [ABSTRACT FROM AUTHOR]