SARS-CoV-2 envelope protein causes acute respiratory distress syndrome (ARDS)-like pathological damages and constitutes an antiviral target

Cytokine storm and multi-organ failure are the main causes of SARS-CoV-2-related death. However, the origin of excessive damages caused by SARS-CoV-2 remains largely unknown. Here we show that the SARS-CoV-2 envelope (2-E) protein alone is able to cause acute respiratory distress syndrome (ARDS)-like damages in vitro and in vivo. 2-E proteins were found to form a type of pH-sensitive cation channels in bilayer lipid membranes. As observed in SARS-CoV-2-infected cells, heterologous expression of 2-E channels induced rapid cell death in various susceptible cell types and robust secretion of cytokines and chemokines in macrophages. Intravenous administration of purified 2-E protein into mice caused ARDS-like pathological damages in lung and spleen. A dominant negative mutation lowering 2-E channel activity attenuated cell death and SARS-CoV-2 production. Newly identified channel inhibitors exhibited potent anti-SARS-CoV-2 activity and excellent cell protective activity in vitro and these activities were positively correlated with inhibition of 2-E channel. Importantly, prophylactic and therapeutic administration of the channel inhibitor effectively reduced both the viral load and secretion of inflammation cytokines in lungs of SARS-CoV-2-infected transgenic mice expressing human angiotensin-converting enzyme 2 (hACE-2). Our study supports that 2-E is a promising drug target against SARS-CoV-2.Subject terms: Cell death, Molecular biology     

TEB/POLQ plays dual roles in protecting Arabidopsis from NO-induced DNA damage

Nitric oxide (NO) is a key player in numerous physiological processes. Excessive NO induces DNA damage, but how plants respond to this damage remains unclear. We screened and identified an Arabidopsis NO hypersensitive mutant and found it to be allelic to TEBICHI/POLQ, encoding DNA polymerase θ. The teb mutant plants were preferentially sensitive to NO- and its derivative peroxynitrite-induced DNA damage and subsequent double-strand breaks (DSBs). Inactivation of TEB caused the accumulation of spontaneous DSBs largely attributed to endogenous NO and was synergistic to DSB repair pathway mutations with respect to growth. These effects were manifested in the presence of NO-inducing agents and relieved by NO scavengers. NO induced G2/M cell cycle arrest in the teb mutant, indicative of stalled replication forks. Genetic analyses indicate that Polθ is required for translesion DNA synthesis across NO-induced lesions, but not oxidation-induced lesions. Whole-genome sequencing revealed that Polθ bypasses NO-induced base adducts in an error-free manner and generates mutations characteristic of Polθ-mediated end joining. Our experimental data collectively suggests that Polθ plays dual roles in protecting plants from NO-induced DNA damage. Since Polθ is conserved in higher eukaryotes, mammalian Polθ may also be required for balancing NO physiological signaling and genotoxicity.     

中微量元素和有益元素对水稻生长和吸收镉的影响

采用盆栽试验,研究了中微量元素和有益元素对水稻生长和吸收镉的影响。结果表明,在所有测试的元素和施用方法中,硅酸钠叶面喷施显著增加稻谷产量,而碳酸钙、硼酸、硅酸钠土施和亚硒酸钠显著降低了稻谷产量。镁、锌、铁的盐酸盐形态对水稻籽粒的增产效果优于硫酸盐形态,而钙、铜的硫酸盐形态增产效果略高于盐酸盐形态。在钙、镁、硫三种中量元素中,钙增加了水稻籽粒中的Cd浓度和吸收量,而镁和硫则降低了籽粒中的Cd浓度和吸收量,以硫磺粉处理为最低。稻草中的Cd浓度和总量均以氯化镁处理为最高,硫磺粉处理最低。镁能有效抑制Cd从秸秆向籽粒的转移,其盐酸盐优于硫酸盐。在微量元素中,锌对水稻Cd的吸收抑制作用最为显著,其次是铜,而有益元素肥料硅酸钠叶面喷施则显著增加了稻谷中的Cd浓度和吸收量。硫酸亚铁、氯化锰、氯化铜、硼酸和硼砂处理都能有效地抑制Cd从秸秆向籽粒的转移,而硅酸钠叶面喷施和锌处理则促进了Cd的转移,表明硅酸钠抑制水稻吸收Cd的机制很可能发生在土壤中,而非在植株体内或地上部分。在Cd污染土壤上选用适宜的中微量和有益元素肥料及其施用方法,能有效降低水稻对镉的吸收和稻米中的Cd含量。     

A secreted ribonuclease effector from Verticillium dahliae localizes in the plant nucleus to modulate host immunity

The arms race between fungal pathogens and plant hosts involves recognition of fungal effectors to induce host immunity. Although various fungal effectors have been identified, the effector functions of ribonucleases are largely unknown. Herein, we identified a ribonuclease secreted by Verticillium dahliae (VdRTX1) that translocates into the plant nucleus to modulate immunity. The activity of VdRTX1 causes hypersensitive response (HR)‐related cell death in Nicotiana benthamiana and cotton. VdRTX1 possesses a signal peptide but is unlikely to be an apoplastic effector because its nuclear localization in the plant is necessary for cell death induction. Knockout of VdRTX1 significantly enhanced V. dahliae virulence on tobacco while V. dahliae employs the known suppressor VdCBM1 to escape the immunity induced by VdRTX1. VdRTX1 homologs are widely distributed in fungi but transient expression of 24 homologs from other fungi did not yield cell death induction, suggesting that this function is specific to the VdRTX1 in V. dahliae. Expression of site‐directed mutants of VdRTX1 in N. benthamiana leaves revealed conserved ligand‐binding sites that are important for VdRTX1 function in inducing cell death. Thus, VdRTX1 functions as a unique HR‐inducing effector in V. dahliae that contributes to the activation of plant immunity.     

极端干旱区尾闾湖生态需水估算——以东居延海为例

以东居延海为研究对象,利用遥感技术目视解译ETM影像,提取东居延海2002—2012年各月湖面面积。通过水文保证率法确定不同保证率下的湖面面积,结合额济纳旗气象站观测的风速、相对湿度、气温、水汽压、降水量等气象数据估算湖泊蒸发耗水量和湖泊降水补给量,根据湖泊渗漏系数估算湖泊渗漏量,最后运用水平衡原理构建湖泊生态需水模型,估算了东居延海在湖面面积保证率为50%、75%、95%时各月月均和年均生态需水量,其中年均生态需水量分别为1.78×108、1.60×108、1.03×108m3,约占莺落峡年均径流量的9.66%、8.66%、5.59%,约占正义峡年均径流量的16.27%、14.60%、9.42%,约占狼心山年均径流量的30.81%、27.65%、17.84%。