农学最新文献

Drought and salt stress are common abiotic constraints that limit plant growth, development, and reproduction. In response, plants have evolved complex molecular regulatory networks enabling them to perceive external stresses acutely and initiate rapid responses. Among these, microRNAs(miRNAs) play a pivotal role. Plant miRNAs are a class of non-coding small RNAs approximately 20-24 nucleotides in length, which exert their stress-responsive functions by cleaving target genes at the post-transcriptional level or inhibiting their translation. In recent years, with the rapid development and widespread application of high-throughput sequencing technology, a large number of miRNAs involved in drought and salt stress responses have been identified, and their functions and mechanisms of action have been gradually elucidated. In this review, we systematically summarize the molecular mechanisms by which miRNAs participate in regulating plant responses to drought and salt stress, comprehensively illustrating the commonality and specificityof miRNA-mediated drought resistance and salt tolerance in plants. We also compile and discuss the miRNAs that could serve as potential targets for biological breeding. The aim is to provide a reference for in-depth research on plant miRNAs, as well as a theoretical basis and forward-looking perspectives for their practical application in the genetic improvement of drought resistance and salt tolerance in plants.

Resistant hypertension (RH) is one of the high-risk types within the spectrum of hypertensive disorders, characterized by a complex pathogenesis. To identify hub differentially expressed genes (DEGs) associated with this disease, this study performed transcriptome sequencing on 30 blood samples collected in 2022 from the Affiliated Hospital of Shandong University of Traditional Chinese Medicine and Jinan Fifth People's Hospital (comprising 10 hypertensive patients, 10 RH patients, and 10 healthy controls). Using DESeq2 analysis, 731 DEGs were initially screened. Subsequently, weighted gene co-expression network analysis (WGCNA) identified 2 modules significantly associated with RH (containing 1,944 genes). Taking the intersection of these module genes and the DEGs yielded 229 key DEGs. Gene Ontology (GO) enrichment analysis revealed that these key DEGs were significantly enriched in biological processes such as drug catabolic process, cellular components like hemoglobin complex, and molecular functions including peroxidase activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that these DEGs were associated with pathways such as the VEGF signaling pathway and mitophagy. A protein-protein interaction (PPI) network was further constructed. Using the cytohubba plugin in Cytoscape software, hub genes were identified by integrating the results from 12 algorithms (taking the intersection of the top 20 genes from each algorithm), preliminarily determining GATA1, EPB42, ANK1, and SNCA as the hub DEGs. Validation by qRT-PCR confirmed that the expression changes of GATA1 and EPB42 were consistent with the sequencing results. This study suggests that the development of RH involves the synergistic action of multiple genes, and perturbations in hub genes (GATA1, EPB42) and related pathways (VEGF signaling pathway, mitophagy) may play significant roles in the disease process. These findings provide new insights for a deeper understanding of the pathological mechanisms underlying RH.

Glutathione peroxidase 8(GPX8) is a key member of the glutathione peroxidase family. Genome-wide association studies (GWAS) have indicated that GPX8 is highly associated with growth and carcass traits of pigs. Using porcine skeletal muscle satellite cells, this study explored the effects of GPX8 on myogenic differentiation and myofiber type switching through GPX8 knockdown and overexpression, combined with analyses involving immunofluorescence staining, qRT-PCR, and Western blotting. The results demonstrated that GPX8 knockdown significantly increased the myogenic differentiation index (P<0.01) and promoted both mRNA and protein levels of the myogenic marker genes MyHC and MyoG (P<0.05). Conversely, GPX8 overexpression exhibited the opposite effects. GPX8 knockdown significantly reduced the mRNA level of MYH7 (P<0.01) and protein level of slow-twitch MyHC (slow-MyHC)(P<0.05), while suppressing mitochondrial biogenesis. In contrast, GPX8 overexpression exhibited opposing results. Integrated multi-omics data from GWAS analyses were employed to identify expression quantitative trait locus (eQTLs) regulating GPX8 expression. The effects of candidate SNPs on GPX8 promoter activity were further validated using dual-luciferase reporter assays. Five candidate SNPs (rs335618489, rs325233940, rs32989756, rs322106839, and rs701033890) were identified within the GPX8 promoter region. Among these, rs335618489-T, rs325233940-G, rs32989756-T, and rs322106839-G significantly upregulated GPX8 expression level by altering promoter activity (P<0.01), thereby influencing porcine muscle development traits. In summary, this study demonstrates that GPX8 inhibits the myogenic differentiation of porcine skeletal muscle satellite cells and promotes the transition from fast-twitch to slow-twitch myofibers. Functional SNPs in the GPX8 promoter region influence porcine muscle development by modulating GPX8 expression, thereby providing valuable breeding targets for improving pork production.

According to the "Prepattern Hypothesis", the development of dorsal sensory organ precursors (SOP) in Drosophila melanogaster depends on the sequential regulation of prepattern genes, proneural genes, and neurogenic genes. In most cases, ectopic SOP formation caused by dysfunction of a single regulatory gene either exhibits spatial discontinuity or is restricted to proneural clusters. However, knockdown of the fred gene induces a novel phenotype of ectopic SOP that are spatially continuous and not confined to proneural cluster regions. This study reveals that fred knockdown-induced ectopic SOP formation is independent of proneural clusters, suggesting that nearly all wing imaginal disc cells possess neurogenic potential. Furthermore, we demonstrate that the prepattern gene pannier (pnr) cooperates with fred to regulate SOP cell fate through two distinct mechanisms: (1) pnr and fred are essential for endogenous SOP formation in the medial notum, while (2) they synergistically suppress SOP initiation outside proneural clusters. These findings challenge the canonical assertion in the "Prepattern Hypothesis" that SOP formation strictly relies on proneural cluster formation, thereby providing a critical extension to the hypothesis.

Sarcopenia is an age-related degenerative disease characterized by progressive loss of skeletal muscle mass and function, resulting severe clinical outcomes such as falls, disability, and increased all-cause mortality, thereby significantly reducing the quality of life in elderly population. With China's rapid demographic aging, sarcopenia is emerging as a critical public health challenge. In this review, we elaborate the pathogenesis of sarcopenia, identifying metabolic imbalance and cellular oxidative stress as major contributing factors to muscle degeneration. Also, this article indicates that life-style, physiological condition and genetic factors jointly influence the population susceptibility and progression of sarcopenia. On one hand, this article lists the non-genetic factors that accelerate the progression of sarcopenia; and on the other hand, it elaborates the role of multiple genes in maintaining muscle function, and the risk associations between genetic mutations and sarcopenia which has been revealed in studies from population cohort and animal models. Moreover, this article summarizes how epigenetic factors regulate muscle metabolism and aging, and comprehensively discusses the intervention effects and clinical limitations of treatment, nutritional support, and exercise therapy. We hope this review can provide a theoretical framework to advance both fundamental research and clinical strategies for sarcopenia prevention and management.

Single nucleotide variants (SNVs) are among the primary pathogenic factors of human genetic diseases, accounting for a significant proportion of all mutation types. Conducting in-depth research on the pathogenic significance of these mutations in animal models is essential for understanding disease mechanisms and developing therapeutic strategies. The progress of such research largely depends on the continuous innovation and advancement of gene editing technologies. In recent years, base editing technology based on the CRISPR/Cas9 system has emerged, enabling precise conversion of individual nucleotides. Owing to its efficiency and convenience, base editing has been widely applied in gene therapy, the construction of animal models, and molecular breeding, bringing new breakthroughs and opportunities to life sciences and medical research. Zebrafish, with their advantages of small size, high fecundity, transparent embryos, and external development, have become an ideal model organism for studying disease mechanisms and drug screening. In this review, we summarize the development of CRISPR/Cas9-based base editing technologies, highlight the emergence of novel editing tools, and explore the application and progress of base editing in constructing precise zebrafish disease models.

Karyotype analysis is a routine prenatal diagnostic procedure in genetic diagnosis and counseling. Chromosomal polymorphisms are frequently observed in karyotyping. However, the absence of standardized criteria for defining polymorphisms has led to inconsistencies across laboratories in determining whether a specific chromosomal variant should be classified as a polymorphism and how it should be symbolized. This lack of consensus hinders the mutual recognition of karyotype reports and complicates the clinical interpretation of polymorphisms. In this expert consensus, we collected cases confirmed of various polymorphic karyotypes, examined their morphological features under different banding techniques, and compared the characteristics of G-, C-, and N-bands across polymorphism types. Based on these comparisons, we established defining features of polymorphic G-bands and categorized the polymorphisms in accordance with the International System for Human Cytogenomic Nomenclature (ISCN 2024). We further propose criteria for the identification, stepwise diagnostic procedures, models for informed consent, and frameworks for clinical interpretation. This consensus aims to standardize the recognition of chromosomal polymorphisms, facilitate the standardization of karyotype reports, promote consistency in genetic counseling, and address long-standing challenges in the field-such as the lack of uniform standards for polymorphism classification and divergent interpretations of the same variant in genetic counseling.