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EDS5 enhanced disease susceptibility 5
Encodes an orphan multidrug and toxin extrusion transporter. Essential component of salicylic acid-dependent signaling for disease resistance. Member of the MATE-transporter family. Expression induced by salicylic acid. Mutants are salicylic acid-deficient. (from
We also demonstrated that the rutin-mediated priming resistance was attenuated in npr1, eds1, eds5, pad4-1, ndr1 mutants, and NahG transgenic Arabidopsis plant, while not in either snc1-11, ein2-5 or jar1 mutants.
Marins et al., Rio Grande, Brazil. In Dis Aquat Organ, Jun 2015
Here, survival was tracked in L. vannamei injected with long synthetic dsRNAs targeted to IMNV open reading frame (ORF) 1a, ORF1b, and ORF2 genome regions prior to injection challenge with IMNV, and real-time RT-PCR was used to track the progress of IMNV infection and mRNA expression levels of the host genes sid1, dicer2, and argonaute2.
Beale et al., Aberystwyth, United Kingdom. In Physiol Plant, 2014
In chilling conditions (5°C), salicylic acid (SA)-deficient mutants (sid2, eds5 and NahG) of Arabidopsis thaliana produced more biomass than wild type (Col-0), whereas the SA overproducer cpr1 was extremely stunted.
Métraux et al., Fribourg, Switzerland. In Bmc Plant Biol, 2014
SA is produced in chloroplasts and the multidrug and toxin extrusion transporter ENHANCED DISEASE SUSCEPTIBILITY5 (EDS5; At4g39030) is necessary for the accumulation of SA after pathogen and abiotic stress.
Deising et al., Halle, Germany. In Mol Microbiol, 2014
eGFP fusions with the key siderophore biosynthesis gene, SID1, encoding l-ornithine-N(5) -monooxygenase, suggested that siderophore biosynthesis is rigorously downregulated specifically during biotrophic development.
Mou et al., Gainesville, United States. In Front Plant Sci, 2013
Complementation tests revealed that seven of the sln mutants are new alleles of eds5/sid1, two are sid2/eds16 alleles, one is allelic to pad4, and the remaining seven sln and two isn mutants are new non-allelic SA accumulation mutants.
Lu et al., Baltimore, United States. In Front Plant Sci, 2013
To further understand how PHT4;1 affects SA accumulation, here we analyzed the genetic interactions between the gain-of-function mutant pht4;1-1 and several known SA mutants, including sid2-1, ald1-1, eds5-3, and pad4-1.
Codd et al., Sydney, Australia. In Metallomics, 2013
Of these metabolites, bioinformatics analysis predicted that S. tropica CNB-440 could potentially biosynthesize, as high affinity Fe(iii) ligands, siderophores from the hydroxamic acid desferrioxamine class (sid1 gene cluster) and the phenolate-thia(oxa)zoli(di)ne class (sid2 and sid4 gene clusters).
Lin et al., Chengdu, China. In Z Naturforsch C, 2013
ABA can down-regulate the expression of the pathogenesis-related genes PR1 and PDF1.2, and compared to the wild type, it drastically reduces TCV accumulation in NahG transgenic plants and the eds5-p1 mutant, both of which do not accumulate SA.