Jasmonate precursor biosynthetic enzymes LOX3 and LOX4 control wound-response growth restriction.

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serval:BIB_1149FE9876BC
Type
Article: article from journal or magazin.
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Publications
Institution
Title
Jasmonate precursor biosynthetic enzymes LOX3 and LOX4 control wound-response growth restriction.
Journal
Plant physiology
Author(s)
Yang T.H., Lenglet-Hilfiker A., Stolz S., Glauser G., Farmer E.E.
ISSN
1532-2548 (Electronic)
ISSN-L
0032-0889
Publication state
Published
Issued date
15/07/2020
Peer-reviewed
Oui
Language
english
Notes
Publication types: Journal Article
Publication Status: aheadofprint
Abstract
Wound-response plant growth restriction requires the synthesis of potent mediators called jasmonates (JAs). Four 13-lipoxygenases (13-LOXs) produce JA precursors in Arabidopsis leaves, but the 13-LOXs responsible for growth restriction have not yet been identified. Through loss-of-function genetic analyses, we identified LOX3 and LOX4 as the principal 13-LOXs responsible for vegetative growth restriction following repetitive wounding. Additional genetic studies were carried out in the gain-of-function fatty acid oxygenation 2 (fou2) mutant that, even when undamaged, shows JA-dependent leaf growth restriction. The fou2 lox3 lox4 triple mutant suppressed the fou2 JA-dependent growth phenotype, confirming that LOX3 and LOX4 function in leaf growth restriction. The fou2 mutation affects the TWO PORE CHANNEL 1 (TPC1) ion channel. Additional genetic approaches based on this gene were used to further investigate LOX3 function in relation to leaf growth. To activate LOX3-dependent JA production in unwounded plants, we employed hyperactive TPC1 variants. Expression of the TPC1ΔCai variant in phloem companion cells caused strongly reduced rosette growth in the absence of wounding. Summarizing, in parallel to their established roles in male reproductive development in Arabidopsis, LOX3 and LOX4 control leaf growth rates after wounding. The process of wound-response growth restriction can be recapitulated in unwounded plants when the LOX3 pathway is activated genetically using a hyperactive vacuolar cation channel.
Pubmed
Open Access
Yes
Create date
24/07/2020 15:14
Last modification date
20/01/2021 8:08
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