Major Latex Protein MdMLP423 Negatively Regulates Defense against Fungal Infections in Apple

Major latex proteins (MLPs) play critical roles in plants defense and stress responses. However, the roles of from apple ( ) have not been clearly identified. In this study, we focused on the biological role of , which had been previously characterized as a potential pathogenesis-related gene. Phylo...

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Published inInternational journal of molecular sciences Vol. 21; no. 5; p. 1879
Main Authors He, Shanshan, Yuan, Gaopeng, Bian, Shuxun, Han, Xiaolei, Liu, Kai, Cong, Peihua, Zhang, Caixia
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 10.03.2020
MDPI
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Summary:Major latex proteins (MLPs) play critical roles in plants defense and stress responses. However, the roles of from apple ( ) have not been clearly identified. In this study, we focused on the biological role of , which had been previously characterized as a potential pathogenesis-related gene. Phylogenetic analysis and conserved domain analysis indicated that is a protein with a 'Gly-rich loop' (GXGGXG) domain belonging to the Bet v_1 subfamily. Gene expression profiles showed that is mainly expressed in flowers. In addition, the expression of was significantly inhibited by f. sp. (BB) and apple pathotype (AAAP) infections. Apple calli overexpressing had lower expression of resistance-related genes, and were more sensitive to infection with BB and AAAP compared with non-transgenic calli. RNA-seq analysis of -overexpressing calli and non-transgenic calli indicated that regulated the expression of a number of differentially expressed genes (DEGs) and transcription factors, including genes involved in phytohormone signaling pathways, cell wall reinforcement, and genes encoding the defense-related proteins, AP2-EREBP, WRKY, MYB, NAC, Zinc finger protein, and ABI3. Taken together, our results demonstrate that negatively regulates apple resistance to BB and AAAP infections by inhibiting the expression of defense- and stress-related genes and transcription factors.
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These authors contributed equally to this work.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms21051879