北部湾鱼类碳、氮、磷生态化学计量特征

为探究北部湾鱼类生态化学计量特征,于2021年3月—4月采集分析了北部湾沿岸9个渔港的79种鱼类(382尾)碳(C)、氮(N)、磷(P)含量特征。结果表明北部湾鱼类C、N、P元素含量变化范围分别为33.87%—58.34%、6.31%—14.92%和0.77%—4.67%;C∶N、C∶P、N∶P的变化范围分别为3.43—9.72、19.15—173.06和5.04—33.68,其中P元素含量变化最大,导致C∶P和N∶P的变化。不同物种在科间的差异较大,科内的差异较小。不同体型和食性鱼类之间的C、N、P含量及比值具有显著差异(P<0.05)。鱼类的C∶P和N∶P与P含量呈显著负相关(R²=0.966,P<0.01;R²=0.877,P<0.01),P含量和Ca含量呈显著正相关(R²=0.919,P<0.01),P含量的变化可能与鱼类骨骼和鳞片的形成有关。总之,北部湾鱼类未保持严格的生态化学计量平衡,鱼类生态化学计量特征存在显著的种间差异,主要因鱼类不同的体型和食性差异所致。     

深渊沉积物中盐单胞菌(Halomonas sp.)NyZ771菌株的分离培养及其降解芳香酸的研究

【背景】海洋是地球上最大的碳库,也是地球生物最大的栖息地。在这个庞大的生态系统中拥有多种多样的微生物,它们在全球碳循环中扮演了重要的角色。海斗深渊(海平面6 000 m以下的海域)由于高静水压和表层沉积汇集了大量有机质,形成了包含丰富生物资源的特殊生境。【目的】从马里亚纳海沟海斗深渊沉积物样品中分离培养能够以芳香酸为唯一碳源和能源生长的微生物,并研究其降解特性。【方法】通过模拟原位高压环境富集培养和常压条件下芳香酸选择性分离培养获得深渊来源的纯培养细菌,并根据形态学观察和16S rRNA基因序列系统发育分析进行种属鉴定,利用不同芳香酸进行培养和生物转化,通过HPLC和LC/MS鉴定芳香酸代谢中间产物。【结果】从马里亚纳海沟6 300 m沉积物样本中分离获得了一株盐单胞菌(Halomonas sp.)NyZ771。该菌株能够利用苯甲酸和4-羟基苯甲酸作为唯一碳源生长。其代谢4-羟基苯甲酸的中间产物鉴定为原儿茶酸。【结论】从深渊沉积物样本分离得到一株能降解苯甲酸和4-羟基苯甲酸的盐单胞菌NyZ771,丰富了深渊来源的微生物资源,为今后研究深渊中微生物的芳香酸降解及海洋微生物驱动的碳循环提供了一定的理论基础。     

内蒙古大青山华北落叶松人工林乔木层碳密度年增量与气象因子的关系

以内蒙古大青山华北落叶松人工林为研究对象,通过树木年轮法和异速生长方程法,计算华北落叶松人工林生物量、碳密度及其年增量的年际变化,并分析碳密度年增量与气温、降水、湿度等气象因子的关系。研究发现：华北落叶松人工林碳密度随着林龄增加的变化曲线可用逻辑斯谛生长方程拟合,在1979—2016年,碳密度由1.05 t/hm~2增加到76.83 t/hm~2。华北落叶松人工林碳密度年增量存在显著的年际差异,总体上呈波动性的“慢-快-慢”趋势,碳密度年增量最高达到3.72 t hm^-2 a^-1,多年平均为2.05 t hm^-2 a^-1。华北落叶松人工林碳密度年增量与上年6月和当年6—8月的降水量显著正相关,与上年11月降水显著负相关;与上年11—12月、当年2月和12月的温度和大气相对湿度分别呈正、负相关;与上年7月、9月及当年8—9月的温度保持显著或极显著正相关。研究表明,温度、湿度和降水主要通过生长季的长短和土壤可利用水分及冬季的雪害冻害影响华北落叶松人工林的碳汇潜力,在未来该地区升温增湿的气候变化趋势下华北...     

母乳微生物及其对婴幼儿健康影响的研究进展

母乳是新生儿最佳的营养来源,不仅提供丰富的营养物质,还能通过自身独特的微生物群影响新生儿肠道细菌的初始定植和机体健康。培养法和基因组测序法均揭示了母乳微生物的多样性和稳定性,除双歧杆菌和乳杆菌外,母乳中还含有多种潜在的益生菌。人乳低聚糖（human milk oligosaccharides,HMOs）是母乳中仅次于乳糖和脂类的第三丰富的营养物质。作为一种天然益生元,HMOs可以选择性地促进有益细菌的生长,从而在促进母乳喂养婴幼儿健康发育方面起着关键作用。本文总结了母乳中微生物的种类、来源、哺乳期间的变化及其与HMOs之间的关系,讨论了母乳微生物对婴幼儿健康的潜在影响,包括抑制病原体入侵肠道、促进免疫系统发育、调节婴幼儿代谢和改善早期认知发育等,以期为母乳源益生菌的开发提供理论指导。

     

Excessive processing and acetylation of OPA1 aggravate age-related hearing loss via the dysregulation of mitochondrial dynamics

The pathogenesis of age-related hearing loss (ARHL) remains unclear. OPA1 is the sole fusion protein currently known to be situated in the inner mitochondrial membrane, which is pivotal for maintaining normal mitochondrial function. While it has already been demonstrated that mutations in OPA1 may lead to hereditary deafness, its involvement in the occurrence and development of ARHL has not been previously explored. In our study, we constructed D-gal-induced senescent HEI-OC1 cells and the cochlea of C57BL/6J mice with a mutated SUMOylation site of SIRT3 using CRISPR/Cas9 technology. We found enhanced L-OPA1 processing mediated by activated OMA1, and increased OPA1 acetylation resulting from reductions in SIRT3 levels in senescent HEI-OC1 cells. Consequently, the fusion function of OPA1 was inhibited, leading to mitochondrial fission and pyroptosis in hair cells, ultimately exacerbating the aging process of hair cells. Our results suggest that the dysregulation of mitochondrial dynamics in cochlear hair cells in aged mice can be ameliorated by activating the SIRT3/OPA1 signaling. This has the potential to alleviate the senescence of cochlear hair cells and reduce hearing loss in mice. Our study highlights the significant roles played by the quantities of long and short chains and the acetylation activity of OPA1 in the occurrence and development of ARHL. This finding offers new perspectives and potential targets for the prevention and treatment of ARHL.     

IL‐33‐ST2 pathway regulates AECII transdifferentiation by targeting alveolar macrophage in a bronchopulmonary dysplasia mouse model

Evidence points to the indispensable function of alveolar macrophages (AMs) in normal lung development and tissue homeostasis. However, the importance of AMs in bronchopulmonary dysplasia (BPD) has not been elucidated. Here, we identified a significant role of abnormal AM proliferation and polarization in alveolar dysplasia during BPD, which is closely related to the activation of the IL‐33‐ST2 pathway. Compared with the control BPD group, AMs depletion partially abolished the epithelialmesenchymal transition process of AECII and alleviated pulmonary differentiation arrest. In addition, IL‐33 or ST2 knockdown has protective effects against lung injury after hyperoxia, which is associated with reduced AM polarization and proliferation. The protective effect disappeared following reconstitution of AMs in injured IL‐33 knockdown mice, and the differentiation of lung epithelium was blocked again. In conclusion, the IL‐33‐ST2 pathway regulates AECII transdifferentiation by targeting AMs proliferation and polarization in BPD, which shows a novel strategy for manipulating the IL‐33–ST2‐AMs axis for the diagnosis and intervention of BPD.     

Rapid improvement of rice eating and cooking quality through gene editing toward glutelin as target

Rice eating and cooking quality(ECQ) is a major concern of breeders and consumers, determining market competitiveness worldwide. Rice grain protein content(GPC) is negatively related to ECQ,making it possible to improve ECQ by manipulating GPC. However, GPC is genetically complex and sensitive to environmental conditions; therefore, little progress has been made in traditional breeding for ECQ. Here, we report that CRISPR/Cas9-mediated knockout of genes encoding the grain storage protein gluteli...     

DNA宏条形码技术在食草动物食性研究中的应用

随着测序技术的快速发展,整合DNA条形码和高通量测序的DNA宏条形码技术已经成为当前研究热点之一,在食草动物的食性鉴定中有很大潜力.放牧动物食性研究是动物营养学和草地生态学领域的重要研究内容.而与传统食性研究方法相比,宏条形码技术可通过对植物DNA条形码的高通量测序,获得样本中的物种组成进而分析动物食性.介绍了传统食性...     

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