The phytohormone jasmonic acid (JA) plays a core role in plant defence against herbivores. When attacked by herbivores, JA and its bioactive derivatives are accumulated at the damage site, and subsequently perceived by the jasmonate co‐receptors COI1 and JAZ proteins. The (+)‐7‐iso‐jasmonoyl‐L‐isoleucine (JA‐Ile) is known to be the main active JA derivative controlling vascular plant responses to herbivores as well as other JA‐regulated processes. However, whether other endogenous JA‐amino acid conjugates (JA‐AAs) are involved in herbivore‐induced defence responses remain unknown. Here, we investigated the role of herbivore‐elicited JA‐AAs in the crop plant rice. The levels of five JA‐AAs were significantly increased under the armyworm, leaf folder and brown planthopper attack. Of the elicited JA derivatives, JA‐Ile, JA‐Val and JA‐Leu could serve as ligands to promote the interaction between rice COI1 and JAZs, inducing OsJAZ4 degradation in vivo. JA‐Val or JA‐Leu treatment increased the expression of JA‐ and defence‐related pathway genes but not JA‐Ile levels, suggesting that these JA‐AAs may directly function in JA signalling. Furthermore, the application of JA‐Val or JA‐Leu resulted in JA‐mediated plant growth inhibition, while enhancing plant resistance to herbivore attack. This study uncovers that JA‐Val and JA‐Leu also play a role in rice defence against herbivores.

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Plant defense against herbivores is costly and often associated with growth repression. The phytohormone jasmonate (JA) plays a central role in prioritizing defense over growth during herbivore attack, but the underlying mechanisms remain unclear. When brown planthoppers (BPH, Nilaparavata lugens) attack rice (Oryza sativa), growth is dramatically suppressed. BPH infestation also increases inactive gibberellin (GA) levels and transcripts of GA 2-oxidase (GA2ox) genes, two (GA2ox3 and GA2ox7) of which encode enzymes that catalyze the conversion of bioactive GAs to inactive GAs in vitro and in vivo. Mutation of these GA2oxs diminishes BPH-elicited growth restriction without affecting BPH resistance. Phytohormone profiling and transcriptome analyses revealed that GA2ox-mediated GA catabolism was enhanced by JA signaling. The transcript levels of GA2ox3 and GA2ox7 were significantly attenuated under BPH attack in JA biosynthesis (allene oxide cyclase, aoc) or signaling-deficient (myc2) mutants. In contrast, GA2ox3 and GA2ox7 expression was increased in MYC2 overexpression lines. MYC2 directly binds to the G-boxes in the promoters of both GA2ox genes to regulate their expression. We conclude that JA signaling simultaneously activates defense responses and GA catabolism to rapidly optimize resource allocation in attacked plants and provides a mechanism for phytohormone crosstalk.

Proper enhancer–promoter interactions are essential to maintaining specific transcriptional patterns and preventing ectopic gene expression. Drosophila is an ideal model organism to study transcriptional regulation due to extensively characterized regulatory regions and the ease of implementing new genetic and molecular techniques for quantitative analysis. The mechanisms of enhancer–promoter interactions have been investigated over a range of length scales. At a DNA level, compositions of both enhancer and promoter sequences affect transcriptional dynamics, including duration, amplitude, and frequency of transcriptional bursting. 3D chromatin topology is also important for proper enhancer–promoter contacts. By working competitively or cooperatively with one another, multiple, simultaneous enhancer–enhancer, enhancer–promoter, and promoter–promoter interactions often occur to maintain appropriate levels of mRNAs. For some long-range enhancer–promoter interactions, extra regulatory elements like insulators and tethering elements are required to promote proper interactions while blocking aberrant ones. This review provides an overview of our current understanding of the mechanism of enhancer–promoter interactions and how perturbations of such interactions affect transcription and subsequent physiological outcomes.