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Obesity-driven cardiac lipid accumulation can progress to lipotoxic cardiomyopathy. Soluble epoxide hydrolase (sEH) is the major enzyme that metabolizes epoxyeicosatrienoic acids (EETs), which have biological activity of regulating lipid metabolism. The current study explores the unknown role of sEH deficiency in lipotoxic cardiomyopathy and its underlying mechanism. Wild-type and Ephx2 knock out (sEH KO) C57BL/6 J mice were fed with high-fat diet (HFD) for 24 weeks to induce lipotoxic cardiomyopathy animal models. Palmitic acid (PA) was utilized to induce lipotoxicity to cardiomyocytes for in vitro study. We found sEH KO, independent of plasma lipid and blood pressures, significantly attenuated HFD-induced myocardial lipid accumulation and cardiac dysfunction in vivo. HFD-induced lipotoxic cardiomyopathy and dysfunction of adenosine 5'-monophosphate-activated protein kinase-mammalian target of rapamycin complex (AMPK-mTORC) signaling mediated lipid autophagy in heart were restored by sEH KO. In primary neonatal mouse cardiomyocytes, both sEH KO and sEH substrate EETs plus sEH inhibitor AUDA treatments attenuated PA-induced lipid accumulation. These effects were blocked by inhibition of AMPK or autophagy. The outcomes were supported by the results that sEH KO and EETs plus AUDA rescued HFD- and PA-induced impairment of autophagy upstream signaling of AMPK-mTORC, respectively. These findings revealed that sEH deficiency played an important role in attenuating myocardial lipid accumulation and provided new insights into treating lipotoxic cardiomyopathy. Regulation of autophagy via AMPK-mTORC signaling pathway is one of the underlying mechanisms.

Cardiovascular diseases (CVDs) are the leading causes of death and disability worldwide, despite the wide diversity of molecular targets identified and the development of therapeutic methods. MicroRNAs (miRNAs) are a class of small (about 22 nucleotides) non-coding RNAs (ncRNAs) that negatively regulate gene expression at the post-transcriptional level in the cytoplasm and play complicated roles in different CVDs. While miRNA overexpression in one type of cell protects against heart disease, it promotes cardiac dysfunction in another type of cardiac cell. Moreover, recent studies have shown that, apart from cytosolic miRNAs, subcellular miRNAs such as mitochondria- and nucleus-localized miRNAs are dysregulated in CVDs. However, the functional properties of cellular- and subcellular-localized miRNAs have not been well characterized. In this review article, by carefully revisiting animal-based miRNA studies in CVDs, we will address the regulation and functional properties of miRNAs in various CVDs. Specifically, the cell–cell crosstalk and subcellular perspective of miRNAs are highlighted. We will provide the background for attractive molecular targets that might be useful in preventing the progression of CVDs and heart failure (HF) as well as insights for future studies.

Improving end-use quality and disease resistance are important goals in wheat breeding. The genetic loci controlling these traits are highly complex, consisting of large families of prolamin and resistance genes with members present in all three homeologous A, B, and D genomes in hexaploid bread wheat. Here, orthologous regions harboring both prolamin and resistance gene loci were reconstructed and compared to understand gene duplication and evolution in different wheat genomes. Comparison of the two orthologous D regions from the hexaploid wheat Chinese Spring and the diploid progenitor Aegilops tauschii revealed their considerable difference due to the presence of five large structural variations with sizes ranging from 100 kb to 2 Mb. As a result, 44% of the Ae. tauschii and 71% of the Chinese Spring sequences in the analyzed regions, including 79 genes, are not shared. Gene rearrangement events, including differential gene duplication and deletion in the A, B, and D regions, have resulted in considerable erosion of gene collinearity in the analyzed regions, suggesting rapid evolution of prolamin and resistance gene families after the separation of the three wheat genomes. We hypothesize that this fast evolution is attributed to the co-evolution of the two gene families dispersed within a high recombination region. The identification of a full set of prolamin genes facilitated transcriptome profiling and revealed that the A genome contributes the least to prolamin expression because of its smaller number of expressed intact genes and their low expression levels, while the B and D genomes contribute similarly.

SUMMARY: Thiamine functions as a crucial activator modulating plant health and broad‐spectrum stress tolerances. However, the role of thiamine in regulating plant virus infection is largely unknown. Here, we report that the multifunctional 17K protein encoded by barley yellow dwarf virus‐GAV (BYDV‐GAV) interacted with barley pyrimidine synthase (HvTHIC), a key enzyme in thiamine biosynthesis. HvTHIC was found to be localized in chloroplast via an N‐terminal 74‐amino acid domain. However, the 17K‐HvTHIC interaction restricted HvTHIC targeting to chloroplasts and triggered autophagy‐mediated HvTHIC degradation. Upon BYDV‐GAV infection, the expression of the HvTHIC gene was significantly induced, and this was accompanied by accumulation of thiamine and salicylic acid. Silencing of HvTHIC expression promoted BYDV‐GAV accumulation. Transcriptomic analysis of HvTHIC silenced and non‐silenced barley plants showed that the differentially expressed genes were mainly involved in plant–pathogen interaction, plant hormone signal induction, phenylpropanoid biosynthesis, starch and sucrose metabolism, photosynthesis‐antenna protein, and MAPK signaling pathway. Thiamine treatment enhanced barley resistance to BYDV‐GAV. Taken together, our findings reveal a molecular mechanism underlying how BYDV impedes thiamine biosynthesis to uphold viral infection in plants. Significance Statement: BYDV‐GAV 17K interacted with barley pyrimidine synthase (HvTHIC), blocked HvTHIC targeting to the chloroplast, and subsequently lead to autophagy‐mediated HvTHIC degradation to disrupt thiamine synthesis, thereby inhibited thiamine mediated defense pathways. [ABSTRACT FROM AUTHOR]

Wheat is one of the most important food crops, both in China and worldwide. Wheat production is facing extreme stresses posed by different diseases, including Fusarium head blight (FHB), which has recently become an increasingly serious concerns. FHB is one of the most significant and destructive diseases affecting wheat crops all over the world. Recent advancements in genomic tools provide a new avenue for the study of virulence factors in relation to the host plants. The current review focuses on recent progress in the study of different strains of Fusarium infection. The presence of genome-wide repeat-induced point (RIP) mutations causes genomic mutations, eventually leading to host plant susceptibility against Fusarium invasion. Furthermore, effector proteins disrupt the host plant resistance mechanism. In this study, we proposed systematic modification of the host genome using modern biological tools to facilitate plant resistance against foreign invasion. We also suggested a number of scientific strategies, such as gene cloning, developing more powerful functional markers, and using haplotype marker-assisted selection, to further improve FHB resistance and associated breeding methods. [ABSTRACT FROM AUTHOR]

Summary: Barley yellow dwarf viruses (BYDVs) cause widespread damage to global cereal crops. Here we report a novel strategy for elevating resistance to BYDV infection. The 17K protein, a potent virulence factor conserved in BYDVs, interacted with barley IMP‐α1 and ‐α2 proteins that are nuclear transport receptors. Consistently, a nuclear localization signal was predicted in 17K, which was found essential for 17K to be transported into the nucleus and to interact with IMP‐α1 and ‐α2. Reducing HvIMP‐α1 and ‐α2 expression by gene silencing attenuated BYDV‐elicited dwarfism, accompanied by a lowered nuclear accumulation of 17K. Among the eight common wheat CRISPR mutants with two to four TaIMP‐α1 and ‐α2 genes mutated, the triple mutant α1aaBBDD/α2AAbbdd and the tetra‐mutant α1aabbdd/α2AAbbDD displayed strong BYDV resistance without negative effects on plant growth under field conditions. The BYDV resistance exhibited by α1aaBBDD/α2AAbbdd and α1aabbdd/α2AAbbDD was correlated with decreased nuclear accumulation of 17K and lowered viral proliferation in infected plants. Our work uncovers the function of host IMP‐α proteins in BYDV pathogenesis and generates the germplasm valuable for breeding BYDV‐resistant wheat. Appropriate reduction of IMP‐α gene expression may be broadly useful for enhancing antiviral resistance in agricultural crops and other economically important organisms. [ABSTRACT FROM AUTHOR]

Achieving high yield and good quality in crops is essential for human food security and health. However, there is usually disharmony between yield and quality. Seed storage protein (SSP) and starch, the predominant components in cereal grains, determine yield and quality, and their coupled synthesis causes a yield–quality trade‐off. Therefore, dissection of the underlying regulatory mechanism facilitates simultaneous improvement of yield and quality. Here, we summarize current findings about the synergistic molecular machinery underpinning SSP and starch synthesis in the leading staple cereal crops, including maize, rice and wheat. We further evaluate the functional conservation and differentiation of key regulators and specify feasible research approaches to identify additional regulators and expand insights. We also present major strategies to leverage resultant information for simultaneous improvement of yield and quality by molecular breeding. Finally, future perspectives on major challenges are proposed. [ABSTRACT FROM AUTHOR]