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KMID : 0381120170390020225
Genes and Genomics
2017 Volume.39 No. 2 p.225 ~ p.236
Transcriptomic profiling of soybean in response to UV-B and Xanthomonas axonopodis treatment reveals shared gene components in stress defense pathways
Yoon Min-Young

Kim Moon-Young
Lee Jayern
Lee Tae-Young
Kim Kil-Hyun
Ha Jung-Min
Kim Yong-Hwan
Lee Suk-Ha
Abstract
Soybean (Glycine max [L.]) has evolved to survive under abiotic and biotic stress conditions by utilizing multiple signaling pathways. Although several studies have revealed shared defense signaling pathways in plants, the majority of components at the convergence points of signaling pathways triggered by both abiotic and biotic stress remain poorly understood. Here, we profiled the overall transcriptional responses of soybean to two different types of stress using the UV-B-resistant cultivar, Buseok, and the UV-B-sensitive cultivar, Cheongja 3, as well as two near isogenic lines carrying bacterial leaf pustule (BLP) disease-resistant and -susceptible alleles. We compared transcript abundance and identified genes that commonly respond to UV-B stress and BLP disease. In addition, we surveyed the co-localization of differentially expressed genes (DEGs) and their paralogs with abiotic and biotic stress-related quantitative trait loci (QTLs) on the soybean genome. Among 14 DEGs that respond to both stresses, five DEGs are involved in the jasmonic acid (JA) metabolic pathway, encoding Jasmonate ZIM (Zinc-finger protein expressed in Inflorescence Meristem) domain-containing protein 1 (JAZ 1), a negative regulator of JA signaling. Two DEGs for JAZ 1 were co-localized with biotic stress-related QTLs. One DEG encoding the stress-induced protein starvation-associated message 22 and its two paralogs were co-localized with both abiotic and biotic stress-related QTLs. The results of this study help elucidate general responses to abiotic and biotic stress in soybean, thereby helping breeders improve stress-resistant soybean cultivars.
KEYWORD
Soybean RNA-seq, UV-B, Bacterial leaf pustule disease, JAZ 1, SAM 22, Shared defense signaling
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