Transcriptome Analysis

转录组分析
  • 文章类型: Journal Article
    可溶性碳水化合物和有机酸是水果风味和消费者偏好的关键决定因素。两者都容易受到采后处理和储存条件的影响。虽然已经确定了1-甲基环丙烯(1-MCP)和非冷冻温度储存在延缓果实成熟和影响风味发展方面的单独有效性,它们对桃贮藏性状的综合影响仍未被探索。本研究考察了1-MCP结合非低温贮藏对黄桃品质和风味特性的影响。我们的结果表明,1-MCP处理通过下调乙烯生物合成和信号基因降低了储存过程中的乙烯产量,并延迟了成熟和软化。转录组学分析表明,1-MCP通过上调蔗糖磷酸合酶(PpSPS1/2)和山梨糖醇脱氢酶(PpSDH1)而下调己糖激酶(PpHXK1)来维持较高水平的可溶性碳水化合物。同时,1-MCP通过抑制乌头合水合酶(PpACO1)和诱导苹果酸脱氢酶(PpMDH1)来保存柠檬酸和苹果酸水平,从而延缓风味降解。共表达网络分析暗示乙烯反应因子(PpERFs)是糖和酸代谢基因的主要调节因子,PpERF19可能作为一个关键的转录控制器。总的来说,本研究验证了1-MCP和非冷冻贮藏组合对黄桃保鲜的有效性,确定了参与糖和酸代谢的关键1-MCP调节基因,并提供了通过采后方法调节桃香发育的见解。
    Soluble carbohydrates and organic acids are critical determinants of fruit flavor and consumer preference, both of which are susceptible to postharvest treatments and storage conditions. While the individual effectiveness of 1-methylcyclopropene (1-MCP) and non-chilling temperature storage in delaying fruit ripening and influencing flavor development has been established, their combined effects on peach storage traits remain unexplored. This study investigated the impact of 1-MCP combined with non-chilling temperature storage on the quality and flavor attributes of yellow peach. Our results revealed that 1-MCP treatment reduced ethylene production during storage and delayed ripening and softening by down-regulating ethylene biosynthesis and signaling genes. Transcriptomic analysis indicated that 1-MCP maintained higher levels of soluble carbohydrates by up-regulating sucrose phosphate synthase (PpSPS1/2) and sorbitol dehydrogenase (PpSDH1) while down-regulating hexokinase (PpHXK1). Concurrently, 1-MCP preserved citric and malic acid levels by suppressing aconitate hydratase (PpACO1) and inducing malate dehydrogenase (PpMDH1), thereby delaying flavor degradation. Co-expression network analysis implicated ethylene response factors (PpERFs) as major regulators of sugar and acid metabolisms genes, with PpERF19 potentially functioning as a key transcriptional controller. Overall, this study verified the efficacy of combined 1-MCP and non-chilling storage for yellow peach preservation, identified key 1-MCP-modulated genes involved in sugar and acid metabolisms, and provided insights into regulating peach flavor development via postharvest approaches.
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  • 文章类型: Journal Article
    为了促进新型农业琥珀酸脱氢酶抑制剂(SDHI)杀菌剂的开发,我们通过将苯基吡唑片段引入吡唑-4-基酰胺的结构中,合成了三个系列的衍生物。生物活性测定结果表明,大多数目标化合物对测试真菌具有不同程度的抑制活性。在100mg/L的浓度下,化合物B8在体内表现出对硬核链球菌的有效保护活性。分子对接分析和琥珀酸脱氢酶(SDH)抑制实验表明B8不是潜在的SDHI。初步的抗真菌机制研究表明,B8诱导菌丝体大量活性氧(ROS)和严重的脂质过氧化损伤,导致菌丝破裂和细胞膜完整性的破坏和可溶性蛋白质的泄漏,可溶性糖和核酸。进一步的转录组分析表明,化合物B8通过下调差异表达基因(DEGs)过氧化氢酶阻断各种代谢途径,破坏过氧化氢水解,加速膜氧化损伤,上调中性神经酰胺酶,加速鞘脂代谢破坏细胞膜结构和细胞增殖和分化,可能加速细胞死亡。以上结果表明,这些双吡唑甲酰胺衍生物的潜在靶标可能是病原真菌的细胞膜。
    To facilitate the development of novel agricultural succinate dehydrogenase inhibitor (SDHI) fungicides, we synthesized three series of derivatives by introducing phenyl pyrazole fragments into the structure of pyrazol-4-yl amides. The results of the bioactivity assay showed that most of the target compounds possessed varying degrees of inhibitory activity against the tested fungi. At a concentration of 100 mg/L, the compound B8 exhibited effective protective activity against S. sclerotiorum in vivo. Molecular docking analysis and succinate dehydrogenase (SDH) inhibition assay indicated that B8 was not a potential SDHI. The preliminary antifungal mechanism of studies showed that B8 induced a large amount of reactive oxygen species (ROS) and severe lipid peroxidation damage in S. sclerotiorum mycelium, resulting in mycelial rupture and disruption of the integrity of the cell membrane and leakage of soluble proteins, soluble sugars and nucleic acids. Further transcriptome analysis showed that compound B8 blocked various metabolic pathways by downregulating the differentially expressed genes (DEGs) catalase, disrupting hydrogen peroxide hydrolysis, accelerating membrane oxidative damage, and upregulating neutral ceramidase, accelerating sphingolipid metabolism to disrupt cell membrane structure and cell proliferation and differentiation, potentially accelerating cell death. The above results indicated that the potential target of these dis-pyrazole carboxamide derivatives may be the cell membrane of pathogenic fungi.
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  • 文章类型: Journal Article
    芒果对低温的高敏感性导致成熟失败,从而限制了产品的适销性。这项研究调查了茉莉酸甲酯(MeJA)对芒果冷藏过程中成熟障碍的影响及其机制。结果显示,50μMMeJA改善了成熟障碍,如加速推进成熟相关参数所示。转录组分析表明,17,414个显著差异表达基因主要富集在乙烯合成中,细胞壁降解,淀粉降解和糖运输。此外,通过qRT-PCR表征了8个AP2/ERF转录因子和12个成熟相关基因。之后,通过对转录因子结合位点和顺式作用元件的分析,构建了由MeJA介导的成熟障碍缓解的ERF调节网络。最后,通过酵母单杂交试验验证了MiERFs与靶基因启动子之间的相互作用。我们的发现为通过抵抗芒果的成熟障碍来提高耐寒性提供了理论依据。
    High susceptibility of mangoes to low temperature leads to ripening failure that restricts the marketability of products. This study investigated the effect of methyl jasmonate (MeJA) on ripening disorder and mechanism involved in mangoes during refrigeration. Results showed that 50 μM MeJA ameliorated ripening disorder, as indicated by accelerated advancement of ripening-related parameters. Transcriptome analysis revealed that 17,414 significantly differentially expressed genes were mainly enriched in ethylene synthesis, cell wall degradation, starch degradation and sugar transport. Moreover, 8 AP2/ERF transcription factors and 12 ripening-related genes were characterized via qRT-PCR. Afterwards, through the analysis of transcription factor binding sites and cis-acting elements, a regulatory network of ERFs mediated alleviation of ripening disorder conferred by MeJA was constructed. Finally, the interactions between MiERFs and the promoters of target genes were verified by yeast one-hybrid assay. Our findings provide a theoretical basis for improving cold tolerance via counteracting ripening disorder in mangoes.
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  • 文章类型: Journal Article
    背景:弓形虫病,弓形虫引起的,给人类和动物带来严重的健康问题。免疫系统受损的个体更容易患严重的弓形虫病。感染弓形虫的孕妇可能面临出生缺陷和流产的可能性。虽然乙胺嘧啶和磺胺嘧啶是临床上常用的药物,对其副作用和阻力的担忧正在上升。从Lycosacoelestis分离的蜘蛛肽XYP1具有有效的抗T。刚地效应,但合成成本高,细胞毒性强。
    方法:本研究旨在修饰XYP1以通过氨基酸截短和取代产生衍生肽。反T.通过锥虫蓝染色法和RH菌株速殖子的杀灭实验评价刚地效应。CCK8和溶血试验用于比较它们的安全性。通过扫描电子显微镜和透射电子显微镜观察弓形虫的形态变化。此外,通过RNA测序进一步探讨XYP1抗弓形虫的机制。
    结果:体内和体外实验表明XYP1-18和XYP1-18-1具有优异的抗T。与XYP1相比,具有更低的细胞毒性和溶血活性。XYP1,XYP1-18和XYP1-18-1能够破坏弓形虫速殖子的表面膜完整性,形成孔隙并导致细胞器的破坏。此外,RNA测序分析表明,XYP1能刺激宿主免疫反应,有效清除弓形虫,减轻宿主的炎症反应。
    结论:XYP1-18比XYP1具有更低的细胞毒性和溶血活性,并能显著延长小鼠的存活时间。XYP1在宿主炎症和免疫反应中发挥作用,揭示其潜在机制。我们的研究为肽基药物的开发和应用提供了有价值的见解,为弓形虫病的治疗提供新的策略和方向。
    BACKGROUND: Toxoplasmosis, caused by Toxoplasma gondii , poses serious health issues for humans and animals. Individuals with impaired immune systems are more susceptible to severe toxoplasmosis. Pregnant women infected by T. gondii can face the possibility of birth defects and miscarriages. While pyrimethamine and sulfadiazine are commonly used drugs in clinical practice, concerns over their side effects and resistance are on the rise. A spider peptide XYP1 isolated from Lycosa coelestis had potent anti-T. gondii effects, but it had a high synthesis cost and strong cytotoxicity.
    METHODS: This study intended to modify XYP1 for producing derived peptides via amino acid truncation and substitution. The anti-T. gondii effect was evaluated by trypan blue staining assay and killing experiment of RH strain tachyzoites. The CCK8 and hemolysis assays were used to compare their safeties. The morphological changes of T. gondii were observed by scanning electron microscope and transmission electron microscope. In addition, the mechanism of XYP1 against T. gondii through RNA-sequencing was further explored.
    RESULTS: In vivo and in vitro experiments revealed that XYP1-18 and XYP1-18-1 had excellent anti-T. gondii activity with lower cytotoxicity and hemolysis activity than XYP1. XYP1, XYP1-18, and XYP1-18-1 were able to disrupt the surface membrane integrity of T. gondii tachyzoites, forming pores and causing the disruption of organelles. Furthermore, RNA-sequencing analysis indicated that XYP1 could stimulate the host immune response to effectively eliminate T. gondii and lessen the host\'s inflammatory reaction.
    CONCLUSIONS: XYP1-18 had lower cytotoxicity and hemolysis activity than XYP1, as well as significantly extending the survival time of the mice. XYP1 played a role in host inflammation and immune responses, revealing its potential mechanism. Our research provided valuable insights into the development and application of peptide-based drugs, offering novel strategies and directions for treating toxoplasmosis.
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  • 文章类型: Journal Article
    煤烟霉菌(SM)病影响生长,植物的发育和代谢,并降低作物的商品和经济价值。SM病是茶树重要的叶部病害之一。尽管如此,关于茶树中SM病的影响的研究很少。在这里,我们发现SM病破坏了细胞的形态和结构,降低了咖啡因的含量,茶氨酸,茶树成熟叶子中的儿茶素。转录组分析表明,SM病抑制了木质素的生物合成,叶绿素,儿茶素,咖啡因,和茶氨酸,并通过下调基因表达影响茶树成熟叶片中植物与病原体的相互作用。此外,两个真菌分离物,MTzyqA和MTzyqB,是从患病茶树的成熟叶子中获得的。通过多基因系统发育分析,将这些菌株鉴定为假枝孢霉,它们在茶树的叶子上附生生长。生防菌JT68、ZGT5和BX1对MTzyqA和MTzyqB有明显的抑制作用。这些结果为了解SM病在茶树中的作用提供了基础。
    Sooty mould (SM) disease affects the growth, development and metabolism of plants and reduces the commodity and economic value of crops. SM disease is one of the important leaf diseases in tea plants. Nonetheless, studies on the effect of SM disease in tea plants are rare. Herein, we found that SM disease disrupted the cell morphology and structure and reduced the contents of caffeine, theanine, and catechins in the mature leaves of tea plants. Transcriptome analysis revealed that SM disease inhibited the biosynthesis of lignin, chlorophyll, catechin, caffeine, and theanine and affected the plant-pathogen interactions in the mature leaves of tea plants by downregulating gene expression. In addition, two fungal isolates, MTzyqA and MTzyqB, were obtained from the mature leaves of diseased tea plants. These strains were identified as Cladosporium pseudocladosporioides by mulitgene phylogenetic analysis, and they grew epiphytically on the leaves of tea plants. The biocontrol bacteria JT68, ZGT5, and BX1 had obvious inhibitory effect on MTzyqA and MTzyqB. These results provide a basis for understanding the effect of SM disease in tea plants.
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  • 文章类型: Journal Article
    在玉米/甘薯中继间作系统中,由于玉米植物的遮荫,早期的弱光胁迫严重限制了甘薯的生长。然而,目前尚不清楚弱光如何影响红薯并导致块茎根流失。通过设置两个光强度级别(弱光=正常光的30%透射率),这项研究在基于田间的实验中评估了两个具有不同耐受性的甘薯品种对弱光的响应,并在基于盆栽的实验中检查了与光和光合作用相关的基因表达的差异。结果表明,在弱光下,功能叶的解剖结构发生了变化,Yuhongxinshu-4和Wanshu-7的叶片厚度分别减少了39.98%和17.32%。S/R比值增加,和根长,根浅表区,根体积都减少了。光合酶rubisco被削弱,净光合速率(Pn)也下降。万树-7的基因表达水平高于于红心树-4。KEGG分析表明,弱光胁迫下两个品种的差异表达基因使用相同的富集途径,主要通过谷胱甘肽代谢和类黄酮生物合成。全光恢复后,差异表达的基因都富集在光合作用等途径中,光合色素合成,和碳代谢。这些发现表明弱光改变了植物的形态,甘薯光合生理及基因表达水平,最终导致块根产量损失。光敏较高的品种(Wanshu-7)对弱光的反应更强。本研究为甘薯耐弱光品种选育和提高继代间作产量提供了理论依据和策略。
    In the relay intercropping system of maize/sweet potato, the growth of the sweet potatoes is seriously limited by weak light stress in the early stage due to shade from maize plants. However, it is not clear how the weak light affects sweet potatoes and causes tuberous root loss. By setting two light intensity levels (weak light = 30% transmittance of normal light), this study evaluated the responses of two sweet potato cultivars with different tolerances to weak light in a field-based experiment and examined the divergence of gene expression related to light and photosynthesis in a pot-based experiment. The results showed that under weak light, the anatomic structure of functional leaves changed, and the leaf thickness decreased by 39.98% and 17.32% for Yuhongxinshu-4 and Wanshu-7, respectively. The ratio of S/R increased, and root length, root superficial area, and root volume all decreased. The photosynthetic enzyme rubisco was weakened, and the net photosynthetic rate (Pn) declined as well. The level of gene expression in Wanshu-7 was higher than that of Yuhongxinshu-4. The KEGG analysis showed that differentially expressed genes from the two cultivars under weak-light stress used the same enrichment pathway, mainly via glutathione metabolism and flavonoid biosynthesis. After full light levels were restored, the differentially expressed genes were all enriched in pathways such as photosynthesis, photosynthetic pigment synthesis, and carbon metabolism. These findings indicated that weak light changed the plant morphology, photosynthetic physiology and gene expression levels of sweet potatoes, which eventually caused losses in the tuberous root yield. The more light-sensitive cultivar (Wanshu-7) had stronger reactions to weak light. This study provides a theoretical basis and strategy for breeding low-light-tolerant varieties and improving relay intercropping production in sweet potatoes.
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  • 文章类型: Journal Article
    为了应对不断变化的气候条件,植物经常面临多种非生物胁迫,需要强大的自适应机制。本研究的重点是SelenicereusundatusL.对两种单独胁迫(镉;镉,盐;S,和干旱;D)及其联合应用,重点是评估(M)褪黑激素的缓解作用。通过转录组分析,这项研究确定了显著的基因表达变化和调控网络激活。结果表明,胁迫使火龙果的生长速率降低30%,将茎和枝条发育减少40%,并在单一和组合应力下增加Cd吸收50%和70%,分别。在应力条件下,H2O2、POD、CAT,APX,SOD和脯氨酸含量升高表明抗氧化能力强。我们确定了141个与应激耐受性相关的常见DEG,其中大部分与AtCBP有关,ALA,和CBP途径。有趣的是,与信号转导和激素相关的基因的产生,包括脱落酸和生长素,也被显著诱导。在M和应激处理期间,几种钙依赖性蛋白激酶基因受到调节。功能富集分析表明,大部分DEGs在代谢过程中富集,MAPK信号,和光合作用。此外,加权基因共表达网络分析(WGCNA)确定了关键转录因子(WRKYs,MYBs,BZIP,bHLHs,和NACs)与抗氧化活性相关,特别是在鲑鱼模块内。本研究提供了火龙果胁迫反应的形态生理和转录组见解,并提出了提高植物抗性的分子育种技术。
    In response to evolving climatic conditions, plants frequently confront multiple abiotic stresses, necessitating robust adaptive mechanisms. This study focuses on the responses of Selenicereus undatus L. to both individual stresses (cadmium; Cd, salt; S, and drought; D) and their combined applications, with an emphasis on evaluating the mitigating effects of (M) melatonin. Through transcriptome analysis, this study identifies significant gene expression changes and regulatory network activations. The results show that stress decreases pitaya growth rates by 30%, reduces stem and cladode development by 40%, and increases Cd uptake under single and combined stresses by 50% and 70%, respectively. Under stress conditions, enhanced activities of H2O2, POD, CAT, APX, and SOD and elevated proline content indicate strong antioxidant defenses. We identified 141 common DEGs related to stress tolerance, most of which were related to AtCBP, ALA, and CBP pathways. Interestingly, the production of genes related to signal transduction and hormones, including abscisic acid and auxin, was also significantly induced. Several calcium-dependent protein kinase genes were regulated during M and stress treatments. Functional enrichment analysis showed that most of the DEGs were enriched during metabolism, MAPK signaling, and photosynthesis. In addition, weighted gene co-expression network analysis (WGCNA) identified critical transcription factors (WRKYs, MYBs, bZIPs, bHLHs, and NACs) associated with antioxidant activities, particularly within the salmon module. This study provides morpho-physiological and transcriptome insights into pitaya\'s stress responses and suggests molecular breeding techniques with which to enhance plant resistance.
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  • 文章类型: Journal Article
    铁是一种重要的微量元素,影响动物的生长发育,调节氧的运输,造血,和缺氧适应。武进猪具有独特的低氧适应性和铁稳态,具体的监管机制鲜有报道。本研究将18只健康乌金仔猪随机分为3组:对照组,补充100mg/kg铁(作为甘氨酸铁);低铁组,不补充铁;高铁组,补充200mg/kg铁(作为甘氨酸铁)。预喂养期为5天,正式期限是30天。在屠宰前和屠宰时从空胃中收集血清,以检测血清铁代谢参数的变化。通过转录组分析分析肝脏中的基因表达,以确定低铁和高铁饮食对转录组水平的影响。对表观血清参数进行相关分析,使用加权基因共表达网络分析进行转录组测序,以揭示低氧调节和铁代谢的关键途径。主要结果如下。(1)除缺氧诱导因子1(HIF-1)含量外(在低铁和高铁组之间),血清铁代谢参数之间未观察到显着差异。低铁组血清HIF-1α含量显著高于高铁组(p<0.05)。(2)肝脏转录组的测序分析显示,低铁组和对照组之间有155个差异表达基因(DEGs),高铁组和对照组之间有229个DEG,以及低铁和高铁组之间的279个DEG。生物信息学分析表明,HIF-1和转化生长因子-β(TGF-β)信号通路是低氧调节和铁代谢的关键通路。选择四个基因进行qPCR验证,结果与转录组测序数据一致。总之,血清铁代谢参数结果表明,在低铁和高铁饮食的影响下,乌金仔猪通过机体复杂的代谢调控维持生理生化指标的稳态,这反映了他们的抗逆性和适应性。转录组结果表明,低铁和高铁饮食对肝脏基因表达水平的影响,表明HIF-1和TGF-β信号通路是调节低铁和高铁饮食下低氧适应性和铁代谢稳态的关键。此外,HIF-1α和HEPC是关键基因。研究结果为探索武进猪铁代谢的调控途径和特征提供了理论基础。
    Iron is an important trace element that affects the growth and development of animals and regulates oxygen transport, hematopoiesis, and hypoxia adaptations. Wujin pig has unique hypoxic adaptability and iron homeostasis; however, the specific regulatory mechanisms have rarely been reported. This study randomly divided 18 healthy Wujin piglets into three groups: the control group, supplemented with 100 mg/kg iron (as iron glycinate); the low-iron group, no iron supplementation; and the high-iron group, supplemented with 200 mg/kg iron (as iron glycinate). The pre-feeding period was 5 days, and the formal period was 30 days. Serum was collected from empty stomachs before slaughter and at slaughter to detect changes in the serum iron metabolism parameters. Gene expression in the liver was analyzed via transcriptome analysis to determine the effects of low- and high-iron diets on transcriptome levels. Correlation analysis was performed for apparent serum parameters, and transcriptome sequencing was performed using weighted gene co-expression network analysis to reveal the key pathways underlying hypoxia regulation and iron metabolism. The main results are as follows. (1) Except for the hypoxia-inducible factor 1 (HIF-1) content (between the low- and high-iron groups), significant differences were not observed among the serum iron metabolic parameters. The serum HIF-1 content of the low-iron group was significantly higher than that of the high-iron group (p < 0.05). (2) Sequencing analysis of the liver transcriptome revealed 155 differentially expressed genes (DEGs) between the low-iron and control groups, 229 DEGs between the high-iron and control groups, and 279 DEGs between the low- and high-iron groups. Bioinformatics analysis showed that the HIF-1 and transforming growth factor-beta (TGF-β) signaling pathways were the key pathways for hypoxia regulation and iron metabolism. Four genes were selected for qPCR validation, and the results were consistent with the transcriptome sequencing data. In summary, the serum iron metabolism parameter results showed that under the influence of low- and high-iron diets, Wujin piglets maintain a steady state of physiological and biochemical indices via complex metabolic regulation of the body, which reflects their stress resistance and adaptability. The transcriptome results revealed the effects of low-iron and high-iron diets on the gene expression level in the liver and showed that the HIF-1 and TGF-β signaling pathways were key for regulating hypoxia adaptability and iron metabolism homeostasis under low-iron and high-iron diets. Moreover, HIF-1α and HEPC were the key genes. The findings provide a theoretical foundation for exploring the regulatory pathways and characteristics of iron metabolism in Wujin pigs.
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  • 文章类型: Journal Article
    (1)研究背景:牛病毒性腹泻病毒(BVDV)引起小牛腹泻,牛呼吸综合征,和母牛流产,给养牛业造成了巨大的经济损失。由于其持续的感染机制,BVDV是牛治疗中的主要挑战。(2)方法:确定二甲双胍(Met)如何抑制BVDV与宿主细胞之间的相互作用,我们用Met处理BVDV感染的细胞。然后,我们对用BVDV感染的Met处理的细胞进行RNA测序(RNA-seq)分析,以鉴定差异表达的基因(DEGs)。因此,通过实时定量PCR(qPCR)验证RNA-seq结果.(3)结果:我们的分析显示Met处理的细胞(Met组)中3169个DEG与用Met(MetBVDV组)预处理后BVDV感染细胞中的阴性对照(NC组)和2510DEGs与BVDV感染的细胞(BVDV组)。在BVDV感染期间,DEGs参与MDBK相互作用,如基因本体论(GO)和京都基因和基因组百科全书(KEGG)途径分析所示。通过蛋白质-蛋白质相互作用(PPI)网络确认了DEGs的潜在相互作用。Met治疗诱导自噬信号活性和自噬相关基因ATG2A的表达,ATG4B,BVDV感染的Met预处理细胞中的ATG10和ATG12。(4)结论:我们发现宿主转录组谱受BVDV感染和Met预处理的影响。这些发现提供了有价值的新见解,并为Met抑制BVDV复制的未来研究提供了支持。
    (1) Background: Bovine viral diarrhea virus (BVDV) causes calf diarrhea, bovine respiratory syndrome, and cow abortion, resulting in substantial economic losses in the cattle industry. Owing to its persistent infection mechanism, BVDV is a major challenge in the treatment of cattle. (2) Methods: To determine how metformin (Met) inhibits the interaction between BVDV and host cells, we treated BVDV-infected cells with Met. We then performed an RNA sequencing (RNA-seq) analysis of Met-treated cells infected with BVDV to identify differentially expressed genes (DEGs). Consequently, the RNA-seq results were validated through real-time quantitative PCR (qPCR). (3) Results: Our analysis revealed 3169 DEGs in the Met-treated cells (Met group) vs. the negative controls (NC group) and 2510 DEGs in the BVDV-infected cells after pretreatment with Met (MetBVDV group) vs. the BVDV-infected cells (BVDV group). The DEGs were involved in MDBK interactions during BVDV infection, as indicated by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. The potential interactions of the DEGs were confirmed via a protein-protein interaction (PPI) network. Met treatment induced autophagy signaling activity and the expression of the autophagy-related genes ATG2A, ATG4B, ATG10, and ATG12 in BVDV-infected Met-pretreated cells. (4) Conclusions: We found that the host transcriptomic profile was affected by BVDV infection and Met pretreatment. These findings offer valuable new insights and provide support for future studies on the inhibition of BVDV replication by Met.
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  • 文章类型: Journal Article
    背景:蜜蜂(Apismellifera),作为农作物的重要传粉者,当使用杀虫剂时存在风险。Sulfoxaflor是一种新型杀虫剂,其作用于烟碱乙酰胆碱受体(nAChR)的方式与新烟碱类相似。这项研究的目的是评估磺胺的毒性及其对A.mellifera暴露的影响。
    结果:最初,发育指标,如幼虫存活,化蛹,5.0mg/L(现场浓度)磺胺抑制了羽化。在蛹期,脂肪含量显著增加,而糖原含量下降。此外,用2.0mg/L(亚致死浓度)的磺胺草胺处理,并通过RNA测序进行分析。转录组结果表明,2.0mg/L量的磺胺对免疫有不利影响,消化性,和神经系统。Sulfoxaflor下调了许多参与免疫的基因的表达,排毒,肌球蛋白细胞骨架,感觉神经元,和气味结合蛋白。
    结论:现场浓度和亚致死浓度用于蜜蜂的联合分析。首次从蜜蜂头转录组测序的角度研究了亚致死浓度磺胺对蜜蜂的影响。对亚致死浓度的磺胺对蜜蜂工人的胁迫进行了初步研究,具有一定的研究意义,可为磺胺在田间环境中的使用提供理论依据。©2024化学工业学会。
    BACKGROUND: Bees (Apis mellifera), as important pollinators of agricultural crops, are at risk when pesticides are used. Sulfoxaflor is a new insecticide which acts on the nicotinic acetylcholine receptor (nAChR) in a similar way to neonicotinoids. The goal of this study is to evaluate the toxicity of sulfoxaflor and its effect on the A. mellifera exposure.
    RESULTS: Initially, developmental indicators such as larval survival, pupation, and eclosion were inhibited by 5.0 mg/L (field concentration) sulfoxaflor. In the pupal stage, fat content was significantly increased, while the glycogen content decreased. In addition, A. mellifera heads were treated with 2.0 mg/L (sublethal concentration) of sulfoxaflor and analyzed by RNA sequencing. The transcriptome results indicated that 2.0 mg/L amounts of sulfoxaflor have adverse effects on the immune, digestive, and nervous systems. Sulfoxaflor down-regulated the expression of many genes involved in immunity, detoxification, the myosin cytoskeleton, sensory neurons, and odor-binding proteins.
    CONCLUSIONS: Field concentration and sublethal concentration were used for the combined analysis of honeybees. The effect of sublethal concentration of sulfoxaflor on honeybees was studied for the first time from the perspective of transcriptome sequencing of honeybee head. A preliminary study was carried out on the stress of sulfoxaflor at sublethal concentration on honeybee workers, which has certain research significance and can provide theoretical basis for the use of sulfoxaflor in the field environment. © 2024 Society of Chemical Industry.
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