黄土高原典型退耕区生态系统服务权衡与协同关系研究——以延安市为例

在退耕还林的背景下,从多尺度分析黄土高原生态系统服务的时空变化及权衡协同关系对促进该区经济发展和生态效益多赢具有重要意义。以黄土高原退耕还林典型区延安市为例,运用InVEST模型评估1988-2018年农作物生产、碳储量、生境质量、土壤保持、产水量5种关键生态系统服务物质量,采用偏相关分析法探讨生态系统服务间的权衡与协同关系及其时空变化特征。研究结果表明：（1）受土地利用变化影响,延安市农作物生产水平、土壤保持年际变化趋势波动较大,农作物生产水平呈波动增加的趋势,土壤保持退耕还林前呈减少,退耕还林后呈波动增加的趋势,碳储量和生境质量呈逐渐增加的趋势,产水量呈逐渐减弱的趋势。（2）生态系统服务与土地利用格局联系紧密。碳储量、生境质量的高值区域以及产水量的低值区域随林地分布格局变化而变化。（3）协同关系是延安市生态系统服务间相关关系的主体,主要发生在碳储量、生境质量、土壤保持、农作物生产之间,权衡关系主要存在于产水量和其他生态系统服务之间。（4）市、县域生态系统服务间关系的差异主要发生在生境质量和土壤保持之间。     

CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis

A major cause of proteinuria in lupus nephritis (LN) is podocyte injury, and determining potential therapeutic targets to prevent podocyte injury is important from a clinical perspective in the treatment of LN. CD36 is involved in podocyte injury in several glomerulopathies and was reported to be a vital candidate gene in LN. Here, we determined the role of CD36 in the podocyte injury of LN and the underlying mechanisms. We observed that CD36 and NLRP3 (NLR family pyrin domain containing 3) were upregulated in the podocytes of lupus nephritis patients and MRL/lpr mice with renal impairment. In vitro, CD36, NLRP3 inflammasome, and autophagy were elevated accompanied with increased podocyte injury stimulated by IgG extracted from lupus nephritis patients compared that from healthy donors. Knocking out CD36 with the CRISPR/cas9 system decreased the NLRP3 inflammasome levels, increased the autophagy levels and alleviated podocyte injury. By enhancing autophagy, NLRP3 inflammasome was decreased and podocyte injury was alleviated. These results demonstrated that, in lupus nephritis, CD36 promoted podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy by enhancing which could decrease NLRP3 inflammasome and alleviate podocyte injury.Subject terms: Mechanisms of disease, Inflammasome, Lupus nephritis, Autophagy     

耦合生态系统服务供需的生态安全格局构建——以苏南地区为例

生态系统服务供需平衡是保障生态安全的基础,将生态系统服务供需作用流动机制融入生态安全格局构建对保障区域生态安全和提升人类生态福祉具有重要意义。基于景观生态学原理,提出耦合生态系统服务供需的生态安全格局构建逻辑方法,以苏南地区为研究区构建了景观生态安全格局和社会生态安全格局。研究结果表明:(1)耦合生态系统服务供需的生态安全格局应以维系区域生态安全和保障区域人类生态福祉为构建目标。其中,生态安全以生态系统服务与生态风险为核心关注对象,人类生态福祉的实现依赖于人类主动获取与生态系统服务流;(2)苏南地区生态系统服务供需间存在错配格局,在此基础上分别识别生态源地与需求源地4247.46km²、1882.16km²,生态廊道与供需廊道1614.02km、1915.82km,生态夹点29处、生态障碍点23处、生态供需节点20处;(3)形成"三区四带两组团"的社会-景观生态安全格局优化布局方案,并在此基础上提出针对性保护修复策略,推动经济-生态空间协同发展。研究可为丰富区域生态安全格局构建理论和方法、推动国土空间优化与管控提供参考借鉴。     

典型海湾与海岛近海脉红螺碳、氮稳定同位素特征差异

为深入了解不同大小脉红螺(Rapana venosa)的碳、氮稳定同位素特征,探究其在典型海湾和海岛水域生态系统所处营养位置,于2022年春季和夏季在胶州湾和长岛近海通过拖网和潜水采集160个脉红螺样本,详细分析了不同体长、体重脉红螺的δ¹³C和δ¹⁵N变化,并计算各研究区域的脉红螺核心生态位宽度及相关参数。结果显示,脉红螺δ¹³C值范围在-22.12‰--16.63‰,四组数据均值为-19.74‰--17.42‰,δ¹⁵N值范围在8.77‰-13.48‰,均值为9.64‰-12.81‰,各组数据营养级均值在2.63-3.57;胶州湾春季脉红螺δ¹³C值与体长、体重呈显著负相关,夏季呈显著正相关,长岛近海区域无明显变化,表明不同季节和不同区域的食物多样性水平存在差异, 胶州湾脉红螺δ¹³C、δ¹⁵N的变化更为突出;两个研究区域δ¹⁵N值和营养级与体长、体重呈显著正相关,主要由于脉红螺摄食偏好性差异,较大的脉红螺倾向于摄食高营养级生物,造成营养级较高。此外,胶州湾脉红螺营养级高于长岛近海,表明其¹⁵N来源更为广泛。营养生态位总面积、δ¹⁵N差值、δ¹³C差值、校正后标准椭圆面积等评价指标,揭示了不同区域、不同季节的脉红螺稳定同位素营养生态位的显著差异,反映了区域地理位置与食物来源对脉红螺δ¹³C和δ¹⁵N的影响。上述研究结果为近海生态系统食物网的构建提供了重要数据,并为区域生物资源的管理和生态系统修复工作提供了科学支撑。     

表观遗传的化学干预对金龟子绿僵菌次生代谢产物影响的研究

[背景] 表观遗传酶类化学抑制剂对真菌的影响研究主要集中在新次生代谢产物挖掘方面,而对大量已知次生代谢物含量的变化却关注较少。金龟子绿僵菌是一种常用杀虫真菌,能代谢出多种已知生物活性物质,其含量可能会影响到该菌与环境间关系及利用潜力。[目的] 评估组蛋白去乙酰化酶和DNA甲基转移酶的化学抑制剂对金龟子绿僵菌代谢物安全性和可利用性的影响。[方法] 在金龟子绿僵菌培养基中添加表观遗传酶类化学抑制剂,培养一定时间后用高分辨液质联用及标准品对照方法分析次生代谢产物变化。根据差异代谢物的生物活性评估化学抑制剂的影响。[结果] 高分辨液质联用分析结果表明当抑制剂浓度达500μmol/L时,金龟子绿僵菌有16种主要次生代谢产物出现明显量的变化,包括destruxin A、A1、A2、B、B1、B2、E、E2、Ed、didesmethyldestruxin C、dihydrodestruxin A、desmethyldestruxin B、12-hydroxyovalicin、subglutinol C、fungerin和ustilagic Acid C。其中,丁酸钠处理可使15种主要代谢物含量升高。苯甲酰胺可使12种主要代谢物含量升高。伏立诺他虽然仅能使10种主要代谢物含量升高,但部分代谢物的升高幅度明显高于前两者。2种DNA甲基转移酶抑制剂可使金龟子绿僵菌代谢物中绿僵菌素类代谢物含量普遍下降。[结论] 组蛋白去乙酰化酶抑制剂可引起金龟子绿僵菌主要代谢物含量普遍升高,而DNA甲基转移酶抑制剂使金龟子绿僵菌的绿僵菌素含量普遍下降。由于变化的代谢物都具有显著的杀虫、免疫抑制或抗菌抗癌等生物活性,因此上述化学抑制剂可增强或降低金龟子绿僵菌对环境中昆虫毒性,同时也增加或降低其代谢物利用潜力。另外,subglutinol C、fungerin和ustilagic Acid C是首次在金龟子绿僵菌中被发现。     

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.     

The Heterogeneity in the Landscape of Gene Dominance in Maize is Accompanied by Unique Chromatin Environments

Subgenome dominance after whole-genome duplication (WGD) has been observed in many plant species. However, the degree to which the chromatin environment affects this bias has not been explored. Here, we compared the dominant subgenome (maize1) and the recessive subgenome (maize2) with respect to patterns of sequence substitutions, genes expression, transposable element accumulation, small interfering RNAs, DNA methylation, histone modifications, and accessible chromatin regions (ACRs). Our data show that the degree of bias between subgenomes for all the measured variables does not vary significantly when both of the WGD genes are located in pericentromeric regions. Our data further indicate that the location of maize1 genes in chromosomal arms is pivotal for maize1 to maintain its dominance, but location has a less effect on maize2 homoeologs. In addition to homoeologous genes, we compared ACRs, which often harbor cis-regulatory elements, between the two subgenomes and demonstrate that maize1 ACRs have a higher level of chromatin accessibility, a lower level of sequence substitution, and are enriched in chromosomal arms. Furthermore, we find that a loss of maize1 ACRs near their nearby genes is associated with a reduction in purifying selection and expression of maize1 genes relative to their maize2 homoeologs. Taken together, our data suggest that chromatin environment and cis-regulatory elements are important determinants shaping the divergence and evolution of duplicated genes.     

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