梨火疫病拮抗菌筛选及温室防效测定

【背景】梨火疫病是由梨火疫病菌(Erwinia amylovora)引起的细菌性病害,对苹果、梨、山楂等40余属220多种植物危害极大。近年来,与中国毗邻的中亚多国相继暴发梨火疫病。梨火疫病菌成为国内特别是对新疆地区的特高风险有害生物,梨火疫病已被中国农业农村部列入《一类农作物病虫害名录》。【目的】从新疆本土材料以及实验室现有菌株中进行梨火疫病菌拮抗菌株的筛选,为梨火疫病的防控奠定基础。【方法】采用平板对峙法从新疆香梨种植区土壤及实验室现有菌株中分离、筛选具有显著拮抗效果的菌株,通过生理生化特性分析和16SrRNA基因测序等方法对菌株进行初步鉴定,并采用牛津杯扩散法对抑菌效果进行复筛。利用两年生盆栽杜梨苗对拮抗菌进行温室内保护型和治疗型防效测定。【结果】筛选获得11株具有显著拮抗作用的菌株,均为革兰氏阳性菌。其中9株为芽胞杆菌属(Bacillus)、2株为乳杆菌属(Lactobacillus)。平板对峙实验结果表明贝莱斯芽胞杆菌(Bacillus velezensis) JE7、植物乳杆菌(Lactobacillus plantarum) LP1和植物乳杆菌LP2拮抗作用较强,其次为贝莱斯芽胞杆菌JE4。生理特性实验结果表明:JE4、JE7可在NaCl浓度为1%-7%时生长,JE4、JE7在pH 4.0-9.0时生长,LP1可在NaCl浓度为1%-9%时生长,在pH 5.0-9.0时生长良好。温室防效测定结果显示,贝莱斯芽胞杆菌JE4防效最佳,可达到73%以上。【结论】筛选获得一批梨火疫病拮抗菌,其中部分菌株在温室内防效显著并具有较强的盐碱耐受能力。     

CircHIPK3 prevents chondrocyte apoptosis and cartilage degradation by sponging miR‐30a‐3p and promoting PON2

Osteoarthritis (OA) is a common joint disease featured by the deterioration of articular cartilage and chondrocyte death. Emerging evidence has indicated that circular RNAs (circRNAs) play an essential role in OA progress. Here, we found that the expression of circHIPK3 was significantly decreased in human and mouse OA cartilage. Knocking down circHIPK3 increased apoptosis and intracellular ROS level in HC‐a chondrocytes. We performed proteomic studies and identified that circHIPK3 regulated chondrocyte apoptosis through the mitochondrial pathway. Results of JC‐1 staining and western blot further confirmed that mitochondrial outer membrane permeabilization was promoted in HC‐a chondrocytes transfected by circHIPK3 siRNA. In terms of mechanism, we showed that PON2 functioned as a potential target of circHIPK3 to regulate chondrocyte apoptosis. Moreover, we revealed that circHIPK3 interacted with miR‐30a‐3p to regulate PON2 expression in chondrocytes. Taken together, our findings suggested that circHIPK3 regulated chondrocyte apoptosis by mitochondrial pathway, and targeting the circHIPK3/miR‐30a‐3p/PON2 axis might be a potential strategy for OA treatment.

The current study revealed the important role of circHIPK3 in regulating chondrocyte apoptosis and maintaining extracellular matrix (ECM) homeostasis. Mechanistically, circHIIPK3 might serve as a sponge of miR‐30a‐3p to regulate PON2 expression. The downregulation of circHIIPK3 resulted in the increased expression of miR‐30a‐3p and decreased expression of PON2, thus leading to mitochondrial pathway apoptosis and ECM destruction.     

Mutant C/EBPα p30 alleviates immunosuppression of CD8+ T cells by inhibiting autophagy‐associated secretion of IL‐1β in AML

ObjectivesMutant C/EBPα p30 (mp30), the product of C/EBPα double mutations (DM), lacks transactivation domain 1 and has C‐terminal loss‐of‐function mutation. Acute myeloid leukaemia (AML) patients harbouring C/EBPα DM could be classified as a distinct subgroup with favourable prognosis. However, the underlying mechanism remains elusive.Materials and MethodsAutophagy regulated by mp30 was detected by western blot and immunofluorescence. Immune infiltration analysis and GSEA were performed to investigate autophagic and inflammatory status of AML patients from the {"type":"entrez-geo","attrs":{"text":"GSE14468","term_id":"14468"}}GSE14468 cohort. Flow cytometry was applied to analyse T cell activation.ResultsMp30 inhibited autophagy by suppressing nucleus translocation of NF‐κB. Autophagy‐associated secretion of IL‐1β was decreased in mp30‐overexpressed AML cells. Bioinformatic analysis revealed that inflammatory status was attenuated, while CD8⁺ T cell infiltration was upregulated in C/EBPα DM AML patients. Consistently, the proportion of CD8⁺CD69⁺ T cells in peripheral blood mononuclear cells (PBMCs) was upregulated after co‐culture with mp30 AML cell conditional culture medium. Knock‐out of IL‐1β in AML cells also enhanced CD8⁺ T cell activation. Accordingly, IL‐1β expression was significantly reduced in the bone marrow (BM) cells of C/EBPα DM AML patients compared to the wildtype, while the CD8⁺CD69⁺ T cell proportion was specifically elevated.ConclusionsC/EBPα DM alleviates immunosuppression of CD8⁺ T cells by inhibiting the autophagy‐associated secretion of IL‐1β, which elucidated that repression of autophagy‐related inflammatory response in AML patients might achieve a favourable clinical benefit.

Mp30 suppresses autophagy‐associated IL‐β secretion, which ultimately alleviates the immunosuppression of CD8⁺ T cells in the microenvironment, contributing to favourable prognosis of AML patients.     

E3 ubiquitin ligase NEDD4L negatively regulates inflammation by promoting ubiquitination of MEKK2

Aberrant activation of inflammation signaling triggered by tumor necrosis factor α (TNF‐α), interleukin‐1 (IL‐1), and interleukin‐17 (IL‐17) is associated with immunopathology. Here, we identify neural precursor cells expressed developmentally down‐regulated gene 4‐like (NEDD4L), a HECT type E3 ligase, as a common negative regulator of signaling induced by TNF‐α, IL‐1, and IL‐17. NEDD4L modulates the degradation of mitogen‐activated protein kinase kinase kinase 2 (MEKK2) via constitutively and directly binding to MEKK2 and promotes its poly‐ubiquitination. In interleukin‐17 receptor (IL‐17R) signaling, Nedd4l knockdown or deficiency enhances IL‐17‐induced p38 and NF‐κB activation and the production of proinflammatory cytokines and chemokines in a MEKK2‐dependent manner. We further show that IL‐17‐induced MEKK2 Ser520 phosphorylation is required not only for downstream p38 and NF‐κB activation but also for NEDD4L‐mediated MEKK2 degradation and the subsequent shutdown of IL‐17R signaling. Importantly, Nedd4l‐deficient mice show increased susceptibility to IL‐17‐induced inflammation and aggravated symptoms of experimental autoimmune encephalomyelitis (EAE) in IL‐17R signaling‐dependent manner. These data suggest that NEDD4L acts as an inhibitor of IL‐17R signaling, which ameliorates the pathogenesis of IL‐17‐mediated autoimmune diseases.     

冬季升温对高山生态系统碳氮循环过程的影响

全球温度升高是目前面临的重要环境问题,但存在明显的季节差异性,即冬季升温幅度显著高于夏季的季节非对称性趋势,这在高纬度和高海拔地区更加显著。冬季升温会直接影响积雪覆盖与冰冻层厚度,并引起冻融交替循环的增加,而冬季植物处于休眠状态,这会直接影响土壤中有效氮的吸收与损失,引起土壤有效氮可利用性的变化。然而,关于冬季增温对后续生长季节植物活动、土壤碳氮循环过程的影响等方面的研究仍存在诸多不确定。综述了冬季升温对积雪覆盖与冻融交替循环改变对高山生态系统物质循环的影响,以及冬季升温对土壤碳氮循环、微生物与酶活性的影响,并由此引起的植物物候期、群落结构、生产与养分循环与凋落物分解等生理、生态过程方面的研究进展。在未来的研究中,应针对不同生态系统特点选择合适的冬季增温方式,加强非极地苔原地区关于冬季升温的研究,注重关注冬季升温对植物-土壤微生物之间反馈作用的影响,重点关注冬季升温对生态系统的延滞效应。     

气候因素对黑线姬鼠种群动态影响的非线性效应

受全球气候变化的影响,气候因素与害鼠种群变化之间的关系成为害鼠防治研究中的热点问题。以西安市长安区周边分布的黑线姬鼠为研究对象,通过标志重捕法进行种群动态监测,掌握其种群数量的动态变化规律,并结合非线性的统计方法广义可加模型,对该地区2015—2018年黑线姬鼠种群密度和气候因素数据进行分析,探讨该鼠种群变化与气候因素之间的关系。结果表明,该地区黑线姬鼠种群数量总体显现为下降趋势。黑线姬鼠种群密度存在显著的正向自我调节效应(F_{1.00, 5.77}=27.062,P<0.01),且与上一月种群密度存在线性的正相关。当月平均温度与该鼠种群密度之间存在显著的非线性效应(F_{1.90, 5.77} =4.696,P<0.05),两者之间显现为钟型关系,当温度<21℃时,两者之间显现为正相关,黑线姬鼠种群密度随温度的升高而升高,反之显现为负相关。当月累计降雨量与其种群密度之间也存在显著的非线性效应(F_{1.87, 5.77}=3.879,P<0.05),同样,两者之间也显现为钟型关系,当降雨量>90 mm时,...     

节肢动物内共生细菌研究进展

节肢动物门是动物界最大的门,占整个动物种数的80%,全世界约有120万现存种。节肢动物在生长发育过程中会感染多种微生物,这些微生物会与其形成协同进化和互利共生的关系。内共生细菌是一类广泛分布于节肢动物体内的共生微生物,能够进行垂直传播和水平传播,对宿主的生长发育、生殖代谢、适应性、免疫功能和进化等诸多方面均具有重要的作用。目前,随着现代分子生物学理论和技术的发展,节肢动物内共生细菌相关研究主要集中在对其宿主的生殖调控功能、与其宿主、宿主寄主植物以及其宿主体内微生物和宿主天敌间互作关系等方面。因此,利用内共生细菌对昆虫种群动态的生殖调控功能,阻断热带蚊虫带来的疾病或植物病害的传播并对宿主昆虫进行种群压制或种群替换,可达到防控害虫的目的。本文从节肢动物内共生细菌的传播方式、对其宿主生物学效应以及内共生细菌与其宿主、宿主寄主植物、宿主天敌和宿主体内微生物互作关系等多方面进行概述,并对内共生细菌今后研究方向进行展望,以期为生物进化、物种形成和种群压制提供参考。     

植物的亲缘选择

亲缘选择是指在一个随机交配群体中的个体基于亲缘关系而以一种非随机性的方式相互作用,其作用结果是亲缘个体得到更大的广义适合度。综述了亲缘选择和亲缘竞争两种观点以及各自的试验支持证据;分析了导致亲缘选择试验结果出现分歧的原因,认为这主要是由于对亲缘选择理解上的模糊以及试验设计的不严谨所致。植物间的亲缘选择研究不仅相对较少,对亲缘选择的机制研究更为欠缺,这就造成了目前对此问题在科学认识上出现不少盲点。综合前期研究,提出今后对亲缘选择的研究应该首先界定"亲缘"程度,同时改良试验设计方案,选择多种不同生境下的物种对亲缘选择进行深入研究,并且考虑环境因子对植物亲缘选择的影响。同时,对植物亲缘识别机制的研究应该从生理生化方面出发,通过定性定量地分析探索植物根系分泌物在植物亲缘识别中的作用和作用途径。     

The connecting cilium inner scaffold provides a structural foundation that protects against retinal degeneration

Inherited retinal degeneration due to loss of photoreceptor cells is a leading cause of human blindness. These cells possess a photosensitive outer segment linked to the cell body through the connecting cilium (CC). While structural defects of the CC have been associated with retinal degeneration, its nanoscale molecular composition, assembly, and function are barely known. Here, using expansion microscopy and electron microscopy, we reveal the molecular architecture of the CC and demonstrate that microtubules are linked together by a CC inner scaffold containing POC5, CENTRIN, and FAM161A. Dissecting CC inner scaffold assembly during photoreceptor development in mouse revealed that it acts as a structural zipper, progressively bridging microtubule doublets and straightening the CC. Furthermore, we show that Fam161a disruption in mouse leads to specific CC inner scaffold loss and triggers microtubule doublet spreading, prior to outer segment collapse and photoreceptor degeneration, suggesting a molecular mechanism for a subtype of retinitis pigmentosa.

Inherited retinal degeneration due to loss of photoreceptor cells is a leading cause of human blindness. Ultrastructure expansion microscopy on mouse retina reveals the presence of a novel structure inside the photoreceptor connecting cilium, the inner scaffold, that protects the outer segment against degeneration.