锰矿区大叶胡枝子灌丛土壤的丛枝菌根真菌多样性

大叶胡枝子(Lespedeza davidii)为一种豆科灌木,具有较强耐受重金属胁迫及固氮能力,也是矿区一种重要修复植物。丛枝菌根真菌(Arbuscular mycorrhizal fungi,AMF)是一类植物共生真菌,它在矿区与植物共生可促进植物生长、提高植物的抗逆性;但其种类、分布及其影响机制尚不够清楚。以大叶胡枝子灌丛土壤AMF群落为研究对象,采集矿区与非矿区大叶胡枝子冠下及其相邻空旷地土壤进行内部转录间隔区(ITS)测序,分析土壤理化性质,揭示不同样地土壤AMF群落的多样性及其影响因素。研究结果表明:(1)土壤样本共得到2961个可操作分类单元(OTU),其中属于AMF的OTU为66个;Silva数据库比对发现AMF有7目10科16属24种。AMF总体物种丰度为矿区相邻空旷地土壤>矿区冠下土壤>非矿区冠下土壤>非矿区相邻空旷地土壤,Shannon指数和Simpson指数与该趋势保持一致。(2)矿区土壤AMF群落以内养囊霉属(Entrophospora)等为优势属,非矿区冠下以斗管囊霉属(Funneliformis)等为优势属。稀有内养囊霉(Entrophospora infrequens)是4个样地共有的优势种,该种为广谱生态型种;Archaeospora sp.和Paraglomerales sp.为矿区冠下的优势种,它们对锰胁迫有较强的耐受性;Funneliformis sp.为非矿区冠下的优势种。(3)冗余分析(RDA)表明,AMF的种类和数量受到锰含量、土壤pH值以及全磷含量的显著影响。本研究结果说明AMF种类及多样性受到土壤理化性质的影响;矿区一些耐性AMF的存在提高了AMF多样性,它们有利于逆境条件下植物的生长。     

高寒半干旱区沙地植被土壤水分变化特征及其影响因素

为揭示高寒半干旱区不同降雨强度对植被差异下沙化土地土壤含水量变化过程的影响。以青海共和盆地东缘黄沙头乔木、灌木和裸地为研究对象,基于2020、2021和2022年5月-9月植物生长季土壤含水量、降雨量和细根分布监测数据,分析2020年、2021年、2022年各生境0-200 cm深度土壤水分对小雨、中雨、大雨的响应。连续动态监测结果表明,大雨、中雨条件下,随土层深度的增加土壤水分对降雨的响应时间延长。乔木林和灌木林土壤水分对中雨、大雨最大响应深度为70 cm、100 cm,裸地对中雨、大雨最大响应深度为50 cm、100 cm。随土层深度的增加,小雨对乔木、灌木、裸地土壤水分的补充作用逐渐降低;中雨对灌木林土壤水分的补充作用逐渐降低,乔木林与之相反;大雨时乔木林、灌木林变异系数呈现S型变化,因此大雨对其土壤水分的补充存在明显的分层利用现象。不同植被类型土壤水分空间变化差异以及对降雨的响应受植被冠层截留对降水再分配的影响,土壤含水量与环境因子间的主成分分析表明,郁闭度、叶面积指数、150-200 cm土壤容重、细根生物量密度、根表面积密度、根长密度、比根长是反映研究区土壤水分的显著因子(P ＜ 0.05)。研究表明不同降雨强度植被土壤含水量存在明显差异,高寒半干旱区沙化土地乔、灌植被的建植可提升深层土壤储水能力;结果可为沙化土地恢复和水土流失防控提供科学依据。     

基于“抗疫精神”的“基因工程”课程思政教学设计与实践

课程思政是当前高校落实“立德树人”根本任务的重要形式。在抗击新型冠状病毒肺炎疫情中,中华民族同舟共济、守望相助,共同铸就了伟大的抗疫精神,为课程思政教学提供了最生动的元素。本文对“战疫”行动中的抗疫精神进行梳理和总结,将其内涵凝练为5项内容;以新型冠状病毒的“核酸检测、疫苗研制及其变异”中蕴含的“抗疫精神”为思政载体,甄选“基因工程”课程中对应的理论内容,开展聚焦抗疫精神的“基因工程”课程思政教学设计与实践研究,利用问卷法和深度访谈法对教学实施效果进行评价,旨在引导学生在学习专业理论知识的同时,感悟课程内容中蕴含的抗疫精神,并将其内化为价值追求,潜移默化中提升学生的思想意识和道德修养,同时为生物类其他专业课程思政教学提供参考和借鉴。     

对生物入侵的几点思考

生物入侵涉及异地迁徙及建群等复杂问题,涉及个体、种群、群落、生态系统等生态学的各个层次,又必不可少地要深入地去探索生物入侵过程中的快速进化和分子生态学基础。生物系统的超级复杂性加上环境和人为因素的极度随机性,充分显示了在这一领域从事研究的艰巨性和挑战性。入侵种具有两面性,因此,预防比治理更为关键。为了应对生物入侵,有待建立完善的国家和地区的防控系统、提高技术水平并加强有关诸多经济因素对生物入侵的影响的研究。     

Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex

Long noncoding RNAs (lncRNAs) play important roles in the spatial and temporal regulation of muscle development and regeneration. Nevertheless, the determination of their biological functions and mechanisms underlying muscle regeneration remains challenging. Here, we identified a lncRNA named lncMREF (lncRNA muscle regeneration enhancement factor) as a conserved positive regulator of muscle regeneration among mice, pigs and humans. Functional studies demonstrated that lncMREF, which is mainly expressed in differentiated muscle satellite cells, promotes myogenic differentiation and muscle regeneration. Mechanistically, lncMREF interacts with Smarca5 to promote chromatin accessibility when muscle satellite cells are activated and start to differentiate, thereby facilitating genomic binding of p300/CBP/H3K27ac to upregulate the expression of myogenic regulators, such as MyoD and cell differentiation. Our results unravel a novel temporal-specific epigenetic regulation during muscle regeneration and reveal that lncMREF/Smarca5-mediated epigenetic programming is responsible for muscle cell differentiation, which provides new insights into the regulatory mechanism of muscle regeneration.     

DNASE1L3 inhibits proliferation,invasion and metastasis of hepatocellular carcinoma by interacting with β‐catenin to promote its ubiquitin degradation pathway

As a member of the deoxyribonuclease 1 family, DNASE1L3 plays a significant role both inside and outside the cell. However, the role of DNASE1L3 in hepatocellular carcinoma (HCC) and its molecular basis remains to be further investigated. In this study, we report that DNASE1L3 is downregulated in clinical HCC samples and evaluate the relationship between its expression and HCC clinical features. In vivo and in vitro experiments showed that DNASE1L3 negatively regulates the proliferation, invasion and metastasis of HCC cells. Mechanistic studies showed that DNASE1L3 recruits components of the cytoplasmic β‐catenin destruction complex (GSK‐3β and Axin), promotes the ubiquitination degradation of β‐catenin, and inhibits its nuclear transfer, thus, decreasing c‐Myc, P21 and P27 level. Ultimately, cell cycle and EMT signals are restrained. In general, this study provides new insight into the mechanism for HCC and suggests that DNASE1L3 can become a considerable target for HCC.

Decreased expression of DNASE1L3 is associated with poor prognosis in patients with HCC DNASE1L3 inhibits the proliferation and cell cycle of HCC cells in vitro and promotes the invasion and metastasis of HCC cells DNASE1L3 inhibits the tumorigenicity and metastasis of HCC cells in vivo DNASE1L3 interacts with β‐catenin and promotes its binding to the β‐catenin destroying complex DNASE1L3 interacts with P21 and stabilizes P21 by mediating the deubiquitin activity     

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.