Arabidopsis <i>CURLY LEAF</i> functions in leaf immunity against fungal pathogens by concomitantly repressing <i>SEPALLATA3</i> and activating <i>ORA59</i>
Arabidopsis <i>CURLY LEAF</i> functions in leaf immunity against fungal pathogens by concomitantly repressing <i>SEPALLATA3</i> and activating <i>ORA59</i>
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拟南芥<i>CURLY LEAF</i>通过同时抑制<i>SEPALLATA3</i>和激活<i>ORA59</i>来发挥叶对真菌病原体的免疫功能
DOI:
10.1111/tpj.15488
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发表时间:
2021
期刊:
影响因子:
--
通讯作者:
Takano Yoshitaka
中科院分区:
文献类型:
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作者:
Singkaravanit‐Ogawa Suthitar;Kosaka Ayumi;Kitakura Saeko;Uchida Kotaro;Nishiuchi Takumi;Ono Erika;Fukunaga Satoshi;Takano Yoshitaka
Arabidopsis non‐host resistance against non‐adapted fungal pathogens includingColletotrichumfungi consists of pre‐invasive and post‐invasive immune responses. Here we report that non‐host resistance against non‐adaptedColletotrichumspp. in Arabidopsis leaves requiresCURLY LEAF(CLF), which is critical for leaf development, flowering and growth. Microscopic analysis of pathogen behavior revealed a requirement forCLFin both pre‐ and post‐invasive non‐host resistance. The loss of a functionalSEPALLATA3(SEP3) gene, ectopically expressed inclfmutant leaves, suppressed not only the defect of theclfplants in growth and leaf development but also a defect in non‐host resistance against the non‐adaptedColletotrichum tropicale. However, the ectopic overexpression ofSEP3in Arabidopsis wild‐type leaves did not disrupt the non‐host resistance. The expression of multiple plant defensin (PDF) genes that are involved in non‐host resistance againstC. tropicalewas repressed inclfleaves. Moreover, theOctadecanoid‐responsive Arabidopsis 59(ORA59) gene, which is required forPDFexpression, was also repressed inclfleaves. Notably, whenSEP3was overexpressed in theora59mutant background,C. tropicaleproduced clear lesions in the inoculated leaves, indicating an impairment in non‐host resistance. Furthermore,ora59plants overexpressingSEP3exhibited a defect in leaf immunity to the adaptedColletotrichum higginsianum. Since theora59plants overexpressingSEP3did not display obvious leaf curling or reduced growth, in contrast to theclfmutants, these results strongly suggest that concomitantSEP3repression andORA59induction via CLF are required for Arabidopsis leaf immunity toColletotrichumfungi, uncoupled from CLF’s function in growth and leaf development.