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Jasmonates regulate transcriptional reprogramming during growth, development, and defense responses. Jasmonoyl-isoleucine, an amino acid conjugate of jasmonic acid (JA), is perceived by the protein complex composed of the F-box protein CORONATINE INSENSITIVE1 (COI1) and JASMONATE ZIM DOMAIN (JAZ) proteins, leading to the ubiquitin-dependent degradation of JAZ proteins. This activates basic helix-loop-helix-type MYC transcription factors to regulate JA-responsive genes. Here, we show that the expression of genes encoding other basic helix-loop-helix transcription factors, JASMONATE ASSOCIATED MYC2-LIKE1 (JAM1), JAM2, and JAM3, is positively regulated in a COI1- and MYC2-dependent manner in Arabidopsis (Arabidopsis thaliana). However, contrary to myc2, the jam1jam2jam3 triple mutant exhibited shorter roots when treated with methyl jasmonate (MJ), indicating enhanced responsiveness to JA. Our genome-wide expression analyses revealed that key jasmonate metabolic genes as well as a set of genes encoding transcription factors that regulate the JA-responsive metabolic genes are negatively regulated by JAMs after MJ treatment. Consistently, loss of JAM genes resulted in higher accumulation of anthocyanin in MJ-treated plants as well as higher accumulation of JA and 12-hydroxyjasmonic acid in wounded plants. These results show that JAMs negatively regulate the JA responses in a manner that is mostly antagonistic to MYC2.

Plants must effectively defend against biotic and abiotic stresses to survive in nature. However, this defense is costly and is often accompanied by significant growth inhibition. How plants coordinate the fluctuating growth-defense dynamics is not well understood and remains a fundamental question. Jasmonate (JA) and gibberellic acid (GA) are important plant hormones that mediate defense and growth, respectively. Binding of bioactive JA or GA ligands to cognate receptors leads to proteasome-dependent degradation of specific transcriptional repressors (the JAZ or DELLA family of proteins), which, at the resting state, represses cognate transcription factors involved in defense (e.g., MYCs) or growth [e.g. phytochrome interacting factors (PIFs)]. In this study, we found that the coi1 JA receptor mutants of rice (a domesticated monocot crop) and Arabidopsis (a model dicot plant) both exhibit hallmark phenotypes of GA-hypersensitive mutants. JA delays GA-mediated DELLA protein degradation, and the della mutant is less sensitive to JA for growth inhibition. Overexpression of a selected group of JAZ repressors in Arabidopsis plants partially phenocopies GA-associated phenotypes of the coi1 mutant, and JAZ9 inhibits RGA (a DELLA protein) interaction with transcription factor PIF3. Importantly, the pif quadruple (pifq) mutant no longer responds to JA-induced growth inhibition, and overexpression of PIF3 could partially overcome JA-induced growth inhibition. Thus, a molecular cascade involving the COI1–JAZ–DELLA–PIF signaling module, by which angiosperm plants prioritize JA-mediated defense over growth, has been elucidated.

Mitochondrial metabolism is an attractive target for cancer therapy 1 , 2 . Reprogramming metabolic pathways could improve the ability of metabolic inhibitors to suppress cancers with limited treatment options, such as triple-negative breast cancer (TNBC) 1 , 3 . Here we show that BTB and CNC homology1 (BACH1) 4 , a haem-binding transcription factor that is increased in expression in tumours from patients with TNBC, targets mitochondrial metabolism. BACH1 decreases glucose utilization in the tricarboxylic acid cycle and negatively regulates transcription of electron transport chain (ETC) genes. BACH1 depletion by shRNA or degradation by hemin sensitizes cells to ETC inhibitors such as metformin 5 , 6 , suppressing growth of both cell line and patient-derived tumour xenografts. Expression of a haem-resistant BACH1 mutant in cells that express a short hairpin RNA for BACH1 rescues the BACH1 phenotype and restores metformin resistance in hemin-treated cells and tumours 7 . Finally, BACH1 gene expression inversely correlates with ETC gene expression in tumours from patients with breast cancer and in other tumour types, which highlights the clinical relevance of our findings. This study demonstrates that mitochondrial metabolism can be exploited by targeting BACH1 to sensitize breast cancer and potentially other tumour tissues to mitochondrial inhibitors. The transcription factor BACH1, which targets mitochondrial metabolism, is expressed at high levels in several types of cancer; reducing its expression in tumours makes them more susceptible to treatment with mitochondrial inhibitors.

\"Young readers will learn to distinguish between the things they really need (food and clothing) and the things they want (toys) in this ... look at wants and needs\"--Publisher marketing.

BackgroundIt is well-known that wasabi constituted mainly 6-(Methylsulfinyl) hexyl isothiocyanate (6-MSITC) has several biological functions on gut health and affects the microbiota. It was recently indicated by several studies that wasabi intake actually affects cardiometabolic health by lowering systolic blood pressure. The study aims to investigate the impact of various factors on the gut microbiota composition and diversity change in the rat model.Methods22 male Wistar rats were kept in separate housing and fed diets high in fat, carbohydrates, and corn starch for 12 weeks. The rats were divided into several treatment groups at random, including control groups, high-carbohydrate, high-fat diet groups, and rats fed a corn starch diet supplemented with wasabi powder. Everyday weight measurements, measurements of the amount of food and water consumed, and the collection of blood and stool samples were made. The rat’s gut microbiota composition was analyzed using advanced techniques ‘Microbiome Analyst’ to get statistical results of different microbial species.ResultsClostridia, mollicutes, Verrucomicrobiae, and deferribacteres have a strong positive correlation with hypertension, and Bacteroidia, Gammaproteobacteria, Actinobacteria, Erysipelotricia, Coriobacteria have a strong negative correlation with hypertension (IDDF2024-ABS-0152-Figure 1. Heatmap of diet intake and its association with microbiome species in different intervention groups). Wasabi intake increases the abundance of Allobaculum and Faecalibaculum (P<0.05). Wasabi intake decreased the abundance of Oscillospira (P<0.05), and there was no significant change in the abundance of Turicibacter (P=0.861) (IDDF2024-ABS-0152-Figure 2. Abundance of Allobaculum Faecalibaculum Oscillibacter Turicibacter in the control group and wasabi intake group). Wasabi intake increases the diversity of specific species of Allobaculum (in genus level), resulting in an increase in the host health of Erysipelotrichia (in feature level), and there was a negative relationship between the Erysipelotrichia species with hypertension (IDDF2024-ABS-0152-Figure 3. Abundance of Erysipelotrichia Allobaculum and Erysipelotrichia in the normal and hypertension group). Clostridia has the largest decrease from 37% to 23% and Erysipelotrichia has the largest increase from 7% to 20% from None and high wasabi intake groups respectively (IDDF2024-ABS-0152-Figure 4. Different microbiome species proportion in wasabi intake left and none wasabi intake right group).Abstract IDDF2024-ABS-0152 Figure 1Heatmap of diet intake and its association with microbiome species in different intervention groupsAbstract IDDF2024-ABS-0152 Figure 2Abundance of allobaculum faecalibaculum oscillibacter turicibacter in the control group and wasabi intake groupAbstract IDDF2024-ABS-0152 Figure 3Abundance of erysipelotrichia allobaculum and erysipelotrichia in the normal and hypertension groupAbstract IDDF2024-ABS-0152 Figure 4Different microbiome species proportion in wasabi intake left and none wasabi intake right groupConclusionsThe study proved that wasabi consumption may lower blood pressure through alterations in the gut microbiota that are related to hypertension in the rat model. Additionally, the study demonstrates that wasabi modifies the gut microbiota’s composition by the abundance of the species Allobaculum and the host health of Erysipeltrichia, which is strongly associated with lowering blood pressure.

\"An EKS book describing the arguments for and against a universal basic income, drawing on research from around the world, with a particular focus on likelihood of adoption within the United States\"-- Provided by publisher.

Sensing and clearance of dysfunctional lysosomes is critical for cellular homeostasis. Here we show that transcription factor EB (TFEB)—a master transcriptional regulator of lysosomal biogenesis and autophagy—is activated during the lysosomal damage response, and its activation is dependent on the function of the ATG conjugation system, which mediates LC3 lipidation. In addition, lysosomal damage triggers LC3 recruitment on lysosomes, where lipidated LC3 interacts with the lysosomal calcium channel TRPML1, facilitating calcium efflux essential for TFEB activation. Furthermore, we demonstrate the presence and importance of this TFEB activation mechanism in kidneys in a mouse model of oxalate nephropathy accompanying lysosomal damage. A proximal tubule-specific TFEB-knockout mouse exhibited progression of kidney injury induced by oxalate crystals. Together, our results reveal unexpected mechanisms of TFEB activation by LC3 lipidation and their physiological relevance during the lysosomal damage response.Nakamura et al. find that the master transcriptional regulator of lysosomal biogenesis and autophagy TFEB is activated following LC3 lipidation during lysosomal damage and show the importance of this mechanism during kidney injury.