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Melatonin‐mediated CcARP1 alters F‐actin dynamics by phosphorylation of CcADF9 to balance root growth and salt tolerance in pigeon pea
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Melatonin‐mediated CcARP1 alters F‐actin dynamics by phosphorylation of CcADF9 to balance root growth and salt tolerance in pigeon pea
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Melatonin‐mediated CcARP1 alters F‐actin dynamics by phosphorylation of CcADF9 to balance root growth and salt tolerance in pigeon pea
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Journal Article
Melatonin‐mediated CcARP1 alters F‐actin dynamics by phosphorylation of CcADF9 to balance root growth and salt tolerance in pigeon pea
2024
Overview
Summary As a multifunctional hormone‐like molecule, melatonin exhibits a pleiotropic role in plant salt stress tolerance. While actin cytoskeleton is essential to plant tolerance to salt stress, it is unclear if and how actin cytoskeleton participates in the melatonin‐mediated alleviation of plant salt stress. Here, we report that melatonin alleviates salt stress damage in pigeon pea by activating a kinase‐like protein, which interacts with an actin‐depolymerizing factor. Cajanus cajan Actin‐Depolymerizing Factor 9 (CcADF9) has the function of severing actin filaments and is highly expressed under salt stress. The CcADF9 overexpression lines (CcADF9‐OE) showed a reduction of transgenic root length and an increased sensitivity to salt stress. By using CcADF9 as a bait to screen an Y2H library, we identified actin depolymerizing factor‐related phosphokinase 1 (ARP1), a novel protein kinase that interacts with CcADF9. CcARP1, induced by melatonin, promotes salt resistance of pigeon pea through phosphorylating CcADF9, inhibiting its severing activity. The CcARP1 overexpression lines (CcARP1‐OE) displayed an increased transgenic root length and resistance to salt stress, whereas CcARP1 RNA interference lines (CcARP1‐RNAi) presented the opposite phenotype. Altogether, our findings reveal that melatonin‐induced CcARP1 maintains F‐actin dynamics balance by phosphorylating CcADF9, thereby promoting root growth and enhancing salt tolerance.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
