基于森林清查资料的河南省森林植被碳储量动态变化

利用1994—1998年、1999—2003年、2004—2008年、2009—2013年河南省4期森林资源清查数据,运用生物量转换因子连续函数法和平均生物量法,估算了1998—2013年河南省森林植被的碳储量和碳密度变化。研究结果表明,河南省森林植被碳储量由1998年的45.57 Tg增加到2013年的107.98 Tg,年均碳汇量为4.16 Tg/a。乔木林碳储量和碳密度分别由1998年的33.54 Tg和22.39 Mg/hm~2增加到2013年的97.11 Tg和31.80 Mg/hm~2。乔木林碳储量在所有植被类型中占主体,4个森林清查时期乔木林碳储量占森林植被总碳储量的比例分别为73.60%、79.22%、85.63%和89.93%。2013年森林清查时,乔木林中杨树和栎类碳储量最大,分别占总碳储量的37.61%和25.22%,各龄组乔木林碳密度大小顺序依次为成熟林近熟林中龄林过熟林幼龄林。阔叶林面积、碳储量、碳密度均高于针叶林,阔叶林是河南省森林碳汇的主要贡献者。人工林面积、碳储量、碳密度增加幅度都要高于天然林,人工林碳储量由1998年的9.62 Tg增加到2013年的55.67 Tg,占乔木林碳储量总增量的77.15%,人工林碳密度由1998年的17.86 Mg/hm~2提高到2013年的32.01 Mg/hm~2,人工林在河南省森林碳汇中逐步发挥重要的作用,逐渐成为河南省森林碳汇的主体,随着人工林生长为具有较高碳密度的成熟林,河南省乔木林将具有较大的碳汇潜力。     

Diet drives convergent evolution of gut microbiomes in bamboo-eating species

Gut microbiota plays a critical role in host physiology and health. The coevolution between the host and its gut microbes facilitates animal adaptation to its specific ecological niche. Multiple factors such as host diet and phylogeny modulate the structure and function of gut microbiota. However, the relative contribution of each factor in shaping the structure of gut microbiota remains unclear. The giant(Ailuropoda melanoleuca) and red(Ailurus styani) pandas belong to different families of order Carnivora. They have evolved as obligate bamboo-feeders and can be used as a model system for studying the gut microbiome convergent evolution. Here, we compare the structure and function of gut microbiota of the two pandas with their carnivorous relatives using 16S rRNA and metagenome sequencing. We found that both panda species share more similarities in their gut microbiota structure with each other than each species shares with its carnivorous relatives. This indicates that the specialized herbivorous diet rather than host phylogeny is the dominant driver of gut microbiome convergence within Arctoidea.Metagenomic analysis revealed that the symbiotic gut microbiota of both pandas possesses a high level of starch and sucrose metabolism and vitamin B12 biosynthesis. These findings suggest a diet-driven convergence of gut microbiomes and provide new insight into host-microbiota coevolution of these endangered species.     

Oxidized high-density lipoprotein promotes CD36 palmitoylation and increases lipid uptake in macrophages

Oxidized high-density lipoprotein (oxHDL) reduces the ability of cells to mediate reverse cholesterol transport and also shows atherogenic properties. Palmitoylation of cluster of differentiation 36 (CD36), an important receptor mediating lipoprotein uptake, is required for fatty acid endocytosis. However, the relationship between oxHDL and CD36 has not been described in mechanistic detail. Here, we demonstrate using acyl-biotin exchange analysis that oxHDL activates CD36 by increasing CD36 palmitoylation, which promotes efficient uptake in macrophages. This modification increased CD36 incorporation into plasma lipid rafts and activated downstream signaling mediators, such as Lyn, Fyn, and c-Jun N-terminal kinase, which elicited enhanced oxHDL uptake and foam cell formation. Furthermore, blocking CD36 palmitoylation with the pharmacological inhibitor 2-bromopalmitate decreased cell surface translocation and lowered oxHDL uptake in oxHDL-treated macrophages. We verified these results by transfecting oxHDL-induced macrophages with vectors expressing wildtype or mutant CD36 (mCD36) in which the cytoplasmic palmitoylated cysteine residues were replaced. We show that cells containing mCD36 exhibited less palmitoylated CD36, disrupted plasma membrane trafficking, and reduced protein stability. Moreover, in ApoE^−/−CD36^−/− mice, lipid accumulation at the aortic root in mice receiving the mCD36 vector was decreased, suggesting that CD36 palmitoylation is responsible for lipid uptake in vivo. Finally, our data indicated that palmitoylation of CD36 was dependent on DHHC6 (Asp-His-His-Cys) acyltransferase and its cofactor selenoprotein K, which increased the CD36/caveolin-1 interaction and membrane targeting in cells exposed to oxHDL. Altogether, our study uncovers a causal link between oxHDL and CD36 palmitoylation and provides insight into foam cell formation and atherogenesis.     

piR-823 inhibits cell apoptosis via modulating mitophagy by binding to PINK1 in colorectal cancer

Mitophagy plays a vital role in the maintenance of mitochondrial homeostasis and tumorigenesis. Noncoding RNA piR-823 contributes to colorectal tumorigenesis. In this study, we aim to evaluate piR-823-mediated mitophagy and its mechanistic association with colorectal cancer (CRC). Digital gene expression analysis was performed to explore the potential functions of piR-823. A piR-823 antagomir (Ant-823) was used to inhibit piR-823 expression, and piR-823 mimics (mimics-823) were used to increase piR-823 expression. Mitophagy was measured in vivo and in vitro by immunofluorescence and western blot analysis. JC-1 staining, ATP production, real-time PCR, and western blot analysis were used to measure changes in mitochondrial quality and number. siRNA transfection was used to inhibit mitophagy, and CCCP was used to induce mitophagy. RNA pull-down assays and RNA-binding protein immunoprecipitation assays were conducted to investigate the molecular mechanisms. Here, we found that CRC cells transfected with Ant-823 presented an altered expression of autophagic and mitophagy genes by Digital gene expression analysis. Ant-823 could promote Parkin activation and mitophagy in vitro and in vivo, followed by mitochondrial loss and dysfunction of some mitochondria, whereas mimics-823 exerted the opposite effects in CRC cells. The inhibition of mitophagy by siParkin alleviated Ant-823-induced mitochondrial loss and dysfunction, as well as apoptosis to a certain extent. Furthermore, piR-823 was found to interact with PINK1 and promote its ubiquitination and proteasome-dependent degradation, thus alleviating mitophagy. Finally, these findings were verifed in samples obtained by patients affected by colorectal cancer. In conclusion, we identify a novel mechanism by which piR-823 regulates mitophagy during CRC tumorigenesis by increasing PINK1 degradation. Subject terms: Colorectal cancer, Gastrointestinal cancer     

森林多目标经营单元的时空尺度扩展

森林多目标经营是我国林业发展的重要趋势,而森林本身的特性以及国内外的众多研究证明,森林多目标经营需要考虑多个时空尺度,以满足其生态、经济和社会效益的综合发挥。在界定多功能林业和森林多目标经营的概念及基础上,系统地分析了传统森林经营时空尺度和现代森林多目标经营时空尺度的联系与区别,提出现代森林多目标经营单元空间尺度上应该满足区域、景观和林分多尺度的需要,而在时间尺度上则要综合考虑短期、中期和长期,并以露水河林业局为例给出具体的研究思路,以期为我国开展森林多目标经营提供借鉴。     

Sulfated glycosaminoglycans and low-density lipoprotein receptor mediate the cellular entry of Clostridium novyi alpha-toxin

Dear Editor, Clostridium novyi(C.novyi)is a spore-forming anaerobic bacterium and opportunistic pathogen causing severe infectious diseases in humans and animal...     

Depression compromises antiviral innate immunity via the AVP-AHI1-Tyk2 axis

Depression is a serious public-health issue. Recent reports have suggested higher susceptibility to viral infections in depressive patients. However, how depression affects antiviral innate immune signaling remains unknown. Here, we revealed a reduction in expression of Abelson helper integration site 1 (AHI1) in the peripheral blood mononuclear cells (PBMCs) and macrophages from the patients with major depressive disorder (MDD), which leads to attenuated antiviral immune response. We found that depression-related arginine vasopressin (AVP) induces reduction of AHI1 in macrophages. Further studies demonstrated that AHI1 is a critical stabilizer of basal type-I-interferon (IFN-I) signaling. Mechanistically, AHI1 recruits OTUD1 to deubiquitinate and stabilize Tyk2, while AHI1 reduction downregulates Tyk2 and IFN-I signaling activity in macrophages from both MDD patients and depression model mice. Interestingly, we identified a clinical analgesic meptazinol that effectively stimulates AHI1 expression, thus enhancing IFN-I antiviral defense in depression model mice. Our study promotes the understanding of the signaling mechanisms of depression-mediated antiviral immune dysfunction, and reveals meptazinol as an enhancer of antiviral innate immunity in depressive patients.Subject terms: Innate immunity, Ubiquitylation, Cell signalling     

水翁(Cleistocalyx operculatus)幼苗对淹水的反应初报

研究了水翁在生理和形态上对3个月淹水期的反应。在潮湿或淹水条件下水翁能存活并保持一定的净光合速率和生长速率,全淹条件下存活期为60d,水翁对淹水的适应包括：（1）淹和的茎部产生肥大皮孔和不定根,（2）不定根系的活力比正常根系的活力高,有不定根的植株的气孔传导率和蒸腾速率比没有不定根的植株高得多。水翁是一种耐淹植物,可在河岸、库岸等水位波动地区种植。     

Direct adenylation from 5′-OH-terminated oligonucleotides by a fusion enzyme containing Pfu RNA ligase and T4 polynucleotide kinase

5′-Adenylated oligonucleotides (AppOligos) are widely used for single-stranded DNA/RNA ligation in next-generation sequencing (NGS) applications such as microRNA (miRNA) profiling. The ligation between an AppOligo adapter and target molecules (such as miRNA) no longer requires ATP, thereby minimizing potential self-ligations and simplifying library preparation procedures. AppOligos can be produced by chemical synthesis or enzymatic modification. However, adenylation via chemical synthesis is inefficient and expensive, while enzymatic modification requires pre-phosphorylated substrate and additional purification. Here we cloned and characterized the Pfu RNA ligase encoded by the PF0353 gene in the hyperthermophilic archaea Pyrococcus furiosus. We further engineered fusion enzymes containing both Pfu RNA ligase and T4 polynucleotide kinase. One fusion enzyme, 8H-AP, was thermostable and can directly catalyze 5′-OH-terminated DNA substrates to adenylated products. The newly discovered Pfu RNA ligase and the engineered fusion enzyme may be useful tools for applications using AppOligos.     

Root developmental responses to phosphorus nutrition

Phosphorus is an essential macronutrient for plant growth and development. Root system architecture (RSA) affects a plant's ability to obtain phosphate, the major form of phosphorus that plants uptake. In this review, I first consider the relationship between RSA and plant phosphorus-acquisition efficiency, describe how external phosphorus conditions both induce and impose changes in the RSA of major crops and of the model plant Arabidopsis, and discuss whether shoot phosphorus status affects RSA and whether there is a universal root developmental response across all plant species. I then summarize the current understanding of the molecular mechanisms governing root developmental responses to phosphorus deficiency. I also explore the possible reasons for the inconsistent results reported by different research groups and comment on the relevance of some studies performed under laboratory conditions to what occurs in natural environments.