Disease relevance of AT3G05510

• This hypersensitivity in ssi2 was rescued by the act1 mutation [1].

High impact information on AT3G05510

• The hydroxyl group in the 3-position of the phenylpropanoid compounds is introduced at the level of coumarate shikimate/quinate esters, whose synthesis implicates an acyltransferase activity [2].
• For functional analysis, the acyltransferase gene was silenced in Arabidopsis thaliana and N. benthamiana by RNA-mediated posttranscriptional gene silencing [2].
• A loss-of-function mutation in the soluble chloroplastic enzyme glycerol-3-phosphate acyltransferase (ACT1) completely reverses SA- and JA-mediated phenotypes in ssi2 [3].
• We previously showed that stearoyl-acyl-carrier-protein-desaturase mutants ssi2/fab2 carrying a loss-of-function mutation in the plastidial glycerol-3-phosphate (G3P) acyltransferase (act1) have elevated 18:1 levels and are restored in their altered defense signaling [1].
• Because G3P is required for the acylation of 18:1 by G3P acyltransferase, it was predicted that reduction of G3P levels should increase 18:1 levels and thereby revert ssi2-triggered phenotypes [1].

Associations of AT3G05510 with chemical compounds

• In contrast to the act1 mutation, a loss-of-function mutation in the endoplasmic reticulum-localized omega6 oleate desaturase (FAD2) does not alter SA- or JA-related phenotypes of ssi2 [3].
• We have characterized a member of the BAHD acyltransferase gene family At3g03480 which catalyzes the formation of (Z)-3-hexen-1-yl acetate from acetyl-CoA and (Z)-3-hexen-1-ol [4].

References