High impact information on Jasmonate

• Analyses of transgenic plants and genome-wide transcript profiling indicated that MKS1 is required for full SA-dependent resistance in mpk4 mutants, and that overexpression of MKS1 in wild-type plants is sufficient to activate SA-dependent resistance, but does not interfere with induction of a defense gene by JA [1].
• Soon after the beginning of singlet oxygen production, the synthesis of oxylipins such as jasmonic acid (JA) and 12-oxophytodienoic acid (OPDA) also start and plants stop growing and induce a cell-death response [2].
• Although the expression of proteinase inhibitor genes in response to JA was inhibited by NO, the expression of wound signaling-associated genes was not [3].
• Arabidopsis plants treated simultaneously with both elictors PehA, known to trigger only JA/ET-dependent defense signaling, and HrpN react with accelerated and enhanced induction of the marker genes PR1 and PDF1.2 both locally and systemically [4].
• This mutual amplification of defense gene expression involves both SA-dependent and JA/ET-dependent defense signaling [4].

Biological context of Jasmonate

• In contrast, expression of mRNA for the zinc finger protein was reduced in the mutants affected in the JA- or SA-dependent pathway [5].
• When the leaf segments were treated with JA in the presence of [Me-2H3]L-methionine, the label was efficiently incorporated into HDMBOA-Glc, while no incorporation into DIMBOA-Glc or HMBOA-Glc was detected, suggesting the conversion of constitutive DIMBOA-Glc to HDMBOA-Glc by methylation at the 4-position [6].

Analytical, diagnostic and therapeutic context of Jasmonate

• These findings suggested that JA functions as a signal transducer in the induction of HDMBOA-Glc accumulation [6].

References