Journal
PLANT CELL AND ENVIRONMENT
Volume 41, Issue 1, Pages 134-147Publisher
WILEY
DOI: 10.1111/pce.12984
Keywords
Mitigen-activated protein kinases; Calcium-dependent protein kinases; Wounding; Ethylene; Arabidopsis
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Funding
- National Natural Science Foundation of China [31272029, 31300244, 31570297]
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Induction of ethylene biosynthesis in response to wounding or herbivores attack is an important part of plant defence response. Here, we identified four ACS isoforms, including ACS2, ACS6, ACS7 and ACS8, contribute to ethylene production in response to wounding. Two independent kinase signalling pathways, MPK3/MPK6 cascade and CPK5/CPK6, are involved in the wounding-induced ethylene biosynthesis via differential regulation of these four ACS genes at transcriptional level. Abstract Ethylene, an important hormone in plant growth, development and response to environmental stimuli, is rapidly induced by mechanical injury or wounding. Although induction of ACS (1-aminocyclopropane-1-carboxylic acid synthase) gene expression has been associated with this process, the detailed regulatory mechanism is unclear. Here, we report that the wounding-induced ethylene production is modulated by both mitogen-activated protein kinase (MAPK) pathway and calcium-dependent protein kinase (CPK) pathway. Study using acs mutants demonstrated that four ACS isoforms, including ACS2, ACS6, ACS7 and ACS8, contribute to ethylene production in response to wounding. Loss-of-function analysis defines the role of MPK3 and MPK6, and their upstream MKK4 and MKK5, in wounding-induced ethylene production. They play an important role in the wounding-induced up-regulation of all four ACS genes expression. Independent of MAPK pathway, CPK5 and CPK6 are also involved in the wounding-induced ethylene production by regulating the expression of ACS2, ACS6 and ACS8 genes. Taken together, we demonstrate that two independent kinase signalling pathways, MPK3/MPK6 cascade and CPK5/CPK6, are involved in the wounding-induced ethylene biosynthesis via differential regulation of ACS genes at transcriptional level.
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