Multi-omic analyses reveal key sectors of jasmonate-mediated defense responses in rice.

The phytohormone jasmonate (JA) plays a central role in plant defenses against biotic stressors. However, our knowledge of the JA signaling pathway in rice (Oryza sativa) remains incomplete. Here, we integrated multi-omic data from three tissues to characterize the functional modules involved in organizing JA-responsive genes. In the core regulatory sector, MYC2 transcription factor transcriptional cascades are conserved. in different species but with distinct regulators (e.g. bHLH6 in rice)., in which genes are early expressed across all tissues. In the feedback sector, MYC2 also regulates the expression of JA repressor and catabolic genes, providing negative feedback that truncates the duration of JA responses. For example, the MYC2-regulated NAC (NAM, ATAF1/2 and CUC2) transcription factor genes NAC1, NAC3, and NAC4 encode proteins that repress JA signaling and herbivore resistance. In the tissue-specific sector, many late-expressed genes are associated with the biosynthesis of specialized metabolites that mediate particular defensive functions. For example, the terpene synthase gene TPS35 is specifically induced in the leaf sheath and TPS35 functions in defense against oviposition by brown planthoppers and the attraction of this herbivore's natural enemies. Thus, by characterizing core, tissue-specific, and feedback sectors of JA-elicited defense responses, this work provides a valuable resource for future discoveries of key JA components in this important crop.

A peroxisomal cinnamate:CoA ligase-dependent phytohormone metabolic cascade in submerged rice germination.

The mechanism underlying the ability of rice to germinate underwater is a largely enigmatic but key research question highly relevant to rice cultivation. Moreover, although rice is known to accumulate salicylic acid (SA), SA biosynthesis is poorly defined, and its role in underwater germination is unknown. It is also unclear whether peroxisomes, organelles essential to oilseed germination and rice SA accumulation, play a role in rice germination. Here, we show that submerged imbibition of rice seeds induces SA accumulation to promote germination in submergence. Two submergence-induced peroxisomal Oryza sativa cinnamate:CoA ligases (OsCNLs) are required for this SA accumulation. SA exerts this germination-promoting function by inducing indole-acetic acid (IAA) catabolism through the IAA-amino acid conjugating enzyme GH3. The metabolic cascade we identified may potentially be adopted in agriculture to improve the underwater germination of submergence-intolerant rice varieties. SA pretreatment is also a promising strategy to improve submerged rice germination in the field.

The N-terminal α2 helix element is critical for the activity of the rice transcription factor MYC2.

Jasmonates (JAs) are a class of phytohormones that play a crucial role in plant growth, development, and environmental stress responses. Central to JA signaling are the MYC2-type transcription factors, as they activate the expression of JA-responsive genes. We previously used CRISPR-Cas9-based genome editing to engineer rice OsMYC2 and yielded a mutant (myc2-5) with a single amino acid (aa) deletion (75I) outside the known functional domains of the protein. This myc2-5 mutant also showed some JA-deficient phenotypes, promoting us to investigate how 75I deletion affects JA responses. The mutation is found in the α2 helix element at the N-terminal of OsMYC2. The deletion of 75I in OsMYC2 rendered plants deficient in most of the JA responses, including root growth, leaf senescence, spikelet development, and resistance to pathogens and herbivores. Biochemical assays revealed that the 75I deletion markedly reduced OsMYC2 protein accumulation, subsequently diminishing its transcriptional activity. However, the deletion did not influence the protein's subcellular localization, DNA-binding capability, or its interactions with JAZ transcriptional repressors and the Mediator complex subunit MED25. Additionally, the screening of seven other deletions in the α2 helix further reinforces the importance of this protein element. Our results highlight the significance of the α2 helix in the N-terminus for OsMYC2's functionality, primarily through modulating its protein levels. This insight expands our knowledge of JA signaling and opens new avenues for research into the yet-to-be-explored domains of the MYC2 protein, with the potential to tailor JA responses in rice and other plant species.

Jasmonate-mediated gibberellin catabolism constrains growth during herbivore attack in rice.

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, Nilaparvata 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, 2 (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.

Unveiling dynamic enhancer-promoter interactions in Drosophila melanogaster.

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.

Epigenome editing and epigenetic gene regulation in disease phenotypes.

Proper gene control across space and time is crucial for the seamless execution of various cellular functions. Rapid advancements in genome-wide studies revealed that in addition to genetic mutations, epigenetic modifications also play an important role in cellular processes and disease development. Epigenetic modifications, including DNA methylation and post-translational modifications on histones via methylation, acetylation, phosphorylation, etc., do not alter DNA sequences. Yet, disruptions of the epigenome can still induce gene malfunction, aberrant cell differentiation, proliferation, and apoptosis, resulting in various diseases such as cancer, neurological disorders, and autoimmune diseases. This review describes the association between epigenetic modifications and disease phenotypes, current techniques to perturb epigenome and analyze changes in gene expression, and perspectives on future epigenetic research.

The jasmonic acid-amino acid conjugates JA-Val and JA-Leu are involved in rice resistance to herbivores.

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.