4.7 Article

Wounding Triggers Wax Biosynthesis in Arabidopsis Leaves in an Abscisic Acid-Dependent and Jasmonoyl-Isoleucine-Dependent Manner

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PLANT AND CELL PHYSIOLOGY
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OXFORD UNIV PRESS
DOI: 10.1093/pcp/pcad137

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Abscisic acid; Arabidopsis thaliana; Drought; Jasmonic acid; Wax; Wounding

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This study investigates the role of wax biosynthesis and respective genes in response to plant wounding. The results show that genes coding for enzymes of surface wax synthesis are induced upon wounding in an ABA-dependent manner. The ABA-dependent transcription factor MYB96 is identified as a key regulator of wax biosynthesis. Furthermore, the study reveals that high humidity prevents wound-induced wax accumulation in Arabidopsis thaliana leaves.
Wounding caused by insects or abiotic factors such as wind and hail can cause severe stress for plants. Intrigued by the observation that wounding induces expression of genes involved in surface wax synthesis in a jasmonoyl-isoleucine (JA-Ile)-independent manner, the role of wax biosynthesis and respective genes upon wounding was investigated. Wax, a lipid-based barrier, protects plants both from environmental threats and from an uncontrolled loss of water. Its biosynthesis is described to be regulated by abscisic acid (ABA), whereas the main wound signal is the hormone JA-Ile. We show in this study that genes coding for enzymes of surface wax synthesis are induced upon wounding in Arabidopsis thaliana leaves in a JA-Ile-independent but an ABA-dependent manner. Furthermore, the ABA-dependent transcription factor MYB96 is a key regulator of wax biosynthesis upon wounding. On the metabolite level, wound-induced wax accumulation is strongly reduced in JA-Ile-deficient plants, but this induction is only slightly decreased in ABA-reduced plants. To further analyze the ABA-dependent wound response, we conducted wounding experiments in high humidity. They show that high humidity prevents the wound-induced wax accumulation in A. thaliana leaves. Together the data presented in this study show that wound-induced wax accumulation is JA-Ile-dependent on the metabolite level, but the expression of genes coding for enzymes of wax synthesis is regulated by ABA.

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