Jasmonates (JAs) are phytohormones with crucial roles in plant defense. Plants accumulate JAs in response to wounding or herbivore attack, but how JA biosynthesis is triggered remains poorly understood. Here we show that herbivory by cotton bollworm (Helicoverpa armigera) induced both ethylene (ET) and JA production in tomato (Solanum lycopersicum) leaves. Using RNA-seq, ET mutants, and inhibitors of ET signaling, we identified ET-induced ETHYLENE RESPONSE FACTOR 15 (ERF15) and ERF16 as critical regulators of JA biosynthesis in tomato plants. Transcripts of ERF15 and ERF16 were markedly upregulated and peaked at 60 and 15 min, respectively, after simulated herbivore attack. While mutation in ERF16 resulted in the attenuated expression of JA biosynthetic genes and decreased JA accumulation 15 min after the simulated herbivory treatment, these changes were not observed in erf15 mutants until 60 min after treatment. Electrophoretic mobility shift assays and dual-luciferase assays demonstrated that both ERFs15 and 16 are transcriptional activators of LIPOXYGENASE D, ALLENE OXIDE CYCLASE, and 12-OXO-PHYTODIENOIC ACID REDUCTASE 3, key genes in JA biosynthesis. Furthermore, JA-activated MYC2 and ERF16 also function as the transcriptional activators of ERF16, contributing to dramatic increases in ERF16 expression. Taken together, our results demonstrated that ET signaling is involved in the rapid induction of the JA burst. ET-induced ERF15 and ERF16 function as powerful transcriptional activators that trigger the JA burst in response to herbivore attack.

The control of apical dominance involves auxin, strigolactones (SLs), cytokinins (CKs), and sugars, but the mechanistic controls of this regulatory network are not fully understood. Here, we show that brassinosteroid (BR) promotes bud outgrowth in tomato through the direct transcriptional regulation of BRANCHED1 (BRC1) by the BR signaling component BRASSINAZOLE-RESISTANT1 (BZR1). Attenuated responses to the removal of the apical bud, the inhibition of auxin, SLs or gibberellin synthesis, or treatment with CK and sucrose, were observed in bud outgrowth and the levels of BRC1 transcripts in the BR-deficient or bzr1 mutants. Furthermore, the accumulation of BR and the dephosphorylated form of BZR1 were increased by apical bud removal, inhibition of auxin, and SLs synthesis or treatment with CK and sucrose. These responses were decreased in the DELLA-deficient mutant. In addition, CK accumulation was inhibited by auxin and SLs, and decreased in the DELLA-deficient mutant, but it was increased in response to sucrose treatment. CK promoted BR synthesis in axillary buds through the action of the type-B response regulator, RR10. Our results demonstrate that BR signaling integrates multiple pathways that control shoot branching. Local BR signaling in axillary buds is therefore a potential target for shaping plant architecture.

Starch is the major storage carbohydrate in plants, and its metabolism in chloroplasts depends mainly on light. However, the mechanism through which photoreceptors regulate starch metabolism in chloroplasts is unclear. In this study, we found that the cryptochrome 1a (CRY1a)-mediated blue light signal is critical for regulating starch accumulation by inducing starch degradation through the HY5 transcription factor in the chloroplasts in tomato. cry1a mutants and HY5-RNAi plants accumulated more starch and presented lower transcript levels of starch degradation-related genes in their leaves than did the wild-type (WT) plants. Blue light significantly induced the transcription of starch degradation-related genes in the wild-type and CRY1a- or HY5-overexpressing plants but had little effect in the cry1a and HY5-RNAi plants. Dual-luciferase assays, electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP)-qPCR revealed that HY5 could activate the starch degradation-related genes PWD, BAM1, BAM3, BAM8, MEX1 and DPE1 by directly binding to their promoters. Silencing of HY5 and these starch degradation-related genes in CRY1a-overexpressing plants led to increased accumulation of starch and decreased accumulation of soluble sugars. These findings presented here not only deepen our understanding of how light control starch degradation and sugar accumulation but also allow us to explore potential targets for improving crop quality.

No abstract

The procedure of preadipocyte differentiation to mature adipocytes is controlled by various transcription factors; these factors activate and regulate the fat formation genes through a series of complex steps. To investigate the time line of gene expression of several potential genes and make a observation, we isolated preadipocytes from subcutaneous adipose tissue of 2-d old piglets by collagenase digestion approach and extracted total RNA from the cells, then measured mRNA expression level of AdipoR1, IGFBP3, PPARγ, PPARGC1, FASN, FABP4, and C/EBPα at 10 different time points via real-time quantitative RT-PCR method. The results revealed that the expression of AdipoR1 and IGFBP3 was both upregulated to the maximum at 8 h, the expression of PPARγ, PPARGC1, FASN, FABP4, and C/EBPα was all upregulated to the maximum at 9 d, and these genes were in significant correlation. We present tentatively conclusions that, the gene expression of AdipoR1 and IGFBP3 is upregulated in the early stage of preadipocyte differentiation, and the gene PPARγ, PPARGC1, FASN, FABP4, and C/EBPα reached a high expression in the later period. The expression variation tendency of these genes suggests that they may influence on each other in a sort of way. However, the specific mechanism that AdipoR1, IGFBP3, PPARγ, and the related genes how to cooperate or interact with each other still remains to be further explored.

Summary Herbivory severely affects plant growth, posing a threat to crop production. Calcium ion (Ca2+) signaling and accumulation of jasmonates (JAs) are activated in plant response to herbivore attack, leading to the expression of defense pathways. However, little is known about how the Ca2+ signal modulates JA biosynthesis. We used diverse techniques, including CRISPR/Cas9, UPLC‐MS/MS and molecular biology methods to explore the role of ETHYLENE RESPONSE FACTOR 16 in Ca2+ signal‐triggered JA burst during herbivore defense in tomato. Here we show that simulated herbivory induces GLUTAMATE RECEPTOR LIKE3.3/3.5 (GLR3.3/3.5)‐dependent increases in electrical activity, Ca2+ influx and increases the abundance of CALMODULIN2 (CaM2) and ERF16 transcripts in tomato. The interaction between CaM2 and ERF16 promotes JA biosynthesis by enhancing the transcriptional activity of ERF16, which increases the activation of ERF16 expression and causes expression of LIPOXYGENASE D (LOXD), AOC and 12‐OXO‐PHYTODIENOIC ACID REDUCTASE 3 (OPR3), the key genes in JA biosynthesis. Mutation of CaM2 results in decreased JA accumulation, together with the expression of JA biosynthesis‐related genes, leading to reduced resistance to the cotton bollworm Helicoverpa armigera. These findings reveal a molecular mechanism underpinning the Ca2+ signal‐initiated systemic JA burst and emphasize the pivotal role of Ca2+ signal/ERF16 crosstalk in herbivore defense.

No abstract

Myosin Va, a member of Class V myosin, functions in organelle motility, spindle formation, nuclear morphogenesis and cell motility. The purpose of this study is to explore the expression and localization of myosin Va in testicular cancer and prostate cancer, and its specific roles in tumor progression including cell division, migration and proliferation. We detected myosin Va in testicular and prostate tumor tissues using sqRT-PCR, western blot, and immunofluorescence. Tumor samples showed an increased expression of myosin Va, abnormal actin and myosin Va distribution. Immunofluorescence images during the cell cycle showed that myosin Va tended to gather at cytoplasm during anaphase but co-localized with nucleus during other phases, suggesting the roles of myosin Va in disassembly of spindle microtubule, movement of chromosomes and normal cytokinesis. In addition, multi-nucleation and aberrant nuclear morphology were observed in myosin Va-knockdown cells. Wounding assay and CCK-8-based cell counting were conducted to explore myosin Va roles in cell migration, viability and proliferation. Our results suggest that myosin Va plays essential roles in maintaining normal mitosis, enhancing tumor cell motility and viability, and these properties are the hallmark of tumor progression and metastasis development. Therefore, an increased understanding of myosin Va expression and function will assist in the development of future oncodiagnosis and -therapy.