薰衣草叶片对低温胁迫的生理与分子响应机制

薰衣草(Lavandula angustifolia)作为名贵的芳香植物,其生长、繁育、品质和产量均受低温影响。前期研究已获得1个耐低温薰衣草品种。该研究将对其处理的温度从20℃降至0℃,揭示薰衣草响应冷胁迫的生理及分子调控机制,同时结合薰衣草的细胞质膜透性、可溶性糖和蛋白质含量及抗氧化酶活性等生理变化。采用转录组学和生物信息学方法挖掘分析相关耐寒基因,并探讨外施水杨酸缓解–10℃冻胁迫的可行性。研究发现7个编码脂肪酸去饱和酶和转移酶的基因(LaFADs)、3个参与合成可溶性糖的基因(LaBAM1和LaSS2)、19个编码胚胎晚期丰富蛋白的基因(LaLEAs)及7个编码过氧化物酶的基因(LaPODs),这些基因在低温胁迫下均上调表达,指导薰衣草合成并积累保护物质,维持膜稳定性以应对胁迫。此外, 150 mg·L^-1水杨酸预处理能有效缓解植株冻害,可作为低温保护剂。该研究丰富了薰衣草重要抗逆基因家族的遗传背景,为后续分子遗传学功能分析和定向品种改良奠定基础。     

不同后作生境对玉米地天敌的冬季保育作用

不同的作物生境可为田间自然天敌提供不同的栖息场所及猎物或寄主,从而影响天敌自身种群的维持及繁衍。在秋收后的玉米地布局不同的作物生境(玉米秸秆生境、叶菜类生境、甘薯生境及杂草带生境),采用目测法和扫网法调查研究其天敌群落组成及时序动态,通过聚类分析探讨了不同作物生境对玉米地自然天敌冬季保育作用的差异性。结果表明,玉米秸秆生境天敌数量最大,共收集天敌555头,约为叶菜类(甘蓝、菜心、油麦菜)生境的2倍,为杂草带和甘薯生境的4.5倍;天敌种类以蜘蛛类群为主,其中甘蓝、甘薯和杂草带生境蜘蛛个体数量占天敌总量的80%以上,而玉米秸秆生境天敌优势种为稻红瓢虫,其种群发生量达30头/100株以上。天敌物种数、多样性指数大小为玉米秸秆生境>叶菜类生境≥杂草带生境>甘薯生境,天敌群落优势度集中性指数与之相反。系统聚类可将6种不同作物生境聚为3类,玉米秸秆生境为一类,叶菜类生境为一类,杂草带和甘薯生境为一类。研究发现,玉米秸秆生境对玉米地天敌的冬季保育作用最佳。     

Exosomal miR-146a-5p and miR-155-5p promote CXCL12/CXCR7-induced metastasis of colorectal cancer by crosstalk with cancer-associated fibroblasts

C-X-C motif chemokine receptor 7 (CXCR7) is a newly discovered atypical chemokine receptor that binds to C-X-C motif chemokine ligand 12 (CXCL12) with higher affinity than CXCR4 and is associated with the metastasis of colorectal cancer (CRC). Cancer-associated fibroblasts (CAFs) have been known to promote tumor progression. However, whether CAFs are involved in CXCR7-mediated metastasis of CRC remains elusive. We found a significant positive correlation between CXCR7 expression and CAF activation markers in colonic tissues from clinical specimens and in villin-CXCR7 transgenic mice. RNA sequencing revealed a coordinated increase in the levels of miR-146a-5p and miR-155-5p in CXCR7-overexpressing CRC cells and their exosomes. Importantly, these CRC cell-derived miR-146a-5p and miR-155-5p could be uptaken by CAFs via exosomes and promote the activation of CAFs through JAK2–STAT3/NF-κB signaling by targeting suppressor of cytokine signaling 1 (SOCS1) and zinc finger and BTB domain containing 2 (ZBTB2). Reciprocally, activated CAFs further potently enhanced the invasive capacity of CRC cells. Mechanistically, CAFs transfected with miR-146a-5p and miR-155-5p exhibited a robust increase in the levels of inflammatory cytokines interleukin-6, tumor necrosis factor-α, transforming growth factor-β, and CXCL12, which trigger the epithelial–mesenchymal transition and pro-metastatic switch of CRC cells. More importantly, the activation of CAFs by miR-146a-5p and miR-155-5p facilitated tumor formation and lung metastasis of CRC in vivo using tumor xenograft models. Our work provides novel insights into CXCR7-mediated CRC metastasis from tumor–stroma interaction and serum exosomal miR-146a-5p and miR-155-5p could serve as potential biomarkers and therapeutic targets for inhibiting CRC metastasis.Subject terms: Cancer microenvironment, Colon cancer     

Construction of disease-specific cytokine profiles by associating disease genes with immune responses

The pathogenesis of many inflammatory diseases is a coordinated process involving metabolic dysfunctions and immune response—usually modulated by the production of cytokines and associated inflammatory molecules. In this work, we seek to understand how genes involved in pathogenesis which are often not associated with the immune system in an obvious way communicate with the immune system. We have embedded a network of human protein-protein interactions (PPI) from the STRING database with 14,707 human genes using feature learning that captures high confidence edges. We have found that our predicted Association Scores derived from the features extracted from STRING’s high confidence edges are useful for predicting novel connections between genes, thus enabling the construction of a full map of predicted associations for all possible pairs between 14,707 human genes. In particular, we analyzed the pattern of associations for 126 cytokines and found that the six patterns of cytokine interaction with human genes are consistent with their functional classifications. To define the disease-specific roles of cytokines we have collected gene sets for 11,944 diseases from DisGeNET. We used these gene sets to predict disease-specific gene associations with cytokines by calculating the normalized average Association Scores between disease-associated gene sets and the 126 cytokines; this creates a unique profile of inflammatory genes (both known and predicted) for each disease. We validated our predicted cytokine associations by comparing them to known associations for 171 diseases. The predicted cytokine profiles correlate (p-value<0.0003) with the known ones in 95 diseases. We further characterized the profiles of each disease by calculating an “Inflammation Score” that summarizes different modes of immune responses. Finally, by analyzing subnetworks formed between disease-specific pathogenesis genes, hormones, receptors, and cytokines, we identified the key genes responsible for interactions between pathogenesis and inflammatory responses. These genes and the corresponding cytokines used by different immune disorders suggest unique targets for drug discovery.     

mTORC1-independent translation control in mammalian cells by methionine adenosyltransferase 2A and S-adenosylmethionine

Methionine adenosyltransferase (MAT) catalyzes the synthesis of S-adenosylmethionine (SAM). As the sole methyl-donor for methylation of DNA, RNA, and proteins, SAM levels affect gene expression by changing methylation patterns. Expression of MAT2A, the catalytic subunit of isozyme MAT2, is positively correlated with proliferation of cancer cells; however, how MAT2A promotes cell proliferation is largely unknown. Given that the protein synthesis is induced in proliferating cells and that RNA and protein components of translation machinery are methylated, we tested here whether MAT2 and SAM are coupled with protein synthesis. By measuring ongoing protein translation via puromycin labeling, we revealed that MAT2A depletion or chemical inhibition reduced protein synthesis in HeLa and Hepa1 cells. Furthermore, overexpression of MAT2A enhanced protein synthesis, indicating that SAM is limiting under normal culture conditions. In addition, MAT2 inhibition did not accompany reduction in mechanistic target of rapamycin complex 1 activity but nevertheless reduced polysome formation. Polysome-bound RNA sequencing revealed that MAT2 inhibition decreased translation efficiency of some fraction of mRNAs. MAT2A was also found to interact with the proteins involved in rRNA processing and ribosome biogenesis; depletion or inhibition of MAT2 reduced 18S rRNA processing. Finally, quantitative mass spectrometry revealed that some translation factors were dynamically methylated in response to the activity of MAT2A. These observations suggest that cells possess an mTOR-independent regulatory mechanism that tunes translation in response to the levels of SAM. Such a system may acclimate cells for survival when SAM synthesis is reduced, whereas it may support proliferation when SAM is sufficient.     

Age‐related memory vulnerability to interfering stimuli is caused by gradual loss of MAPK‐dependent protection in Drosophila

Age‐related memory impairment (AMI) is a common phenomenon across species. Vulnerability to interfering stimuli has been proposed to be an important cause of AMI. However, the molecular mechanisms underlying this vulnerability‐related AMI remain unknown. Here we show that learning‐activated MAPK signals are gradually lost with age, leading to vulnerability‐related AMI in Drosophila. Young flies (2‐ or 3‐day‐old) exhibited a significant increase in phosphorylated MAPK levels within 15 min after learning, whereas aged flies (25‐day‐old) did not. Compared to 3‐day‐old flies, significant 1 h memory impairments were observed in 15‐, 20‐, and 30‐day‐old flies, but not in 10‐day‐old flies. However, with post‐learning interfering stimuli such as cooling or electric stimuli, 10‐day‐old flies had worse memory performance at 1 h than 3‐day‐old flies, showing a premature AMI phenomenon. Increasing learning‐activated MAPK signals through acute transgene expression in mushroom body (MB) neurons restored physiological trace of 1 h memory in a pair of MB output neurons in aged flies. Decreasing such signals in young flies mimicked the impairment of 1 h memory trace in aged flies. Restoring learning‐activated MAPK signals in MB neurons in aged flies significantly suppressed AMI even with interfering stimuli. Thus, our data suggest that age‐related loss of learning‐activated neuronal MAPK signals causes memory vulnerability to interfering stimuli, thereby leading to AMI.     

大气氟污染对达乌尔黄鼠及其环境的影响

本文研究大气氟污染对达乌尔黄鼠及其环境的影响。研究区内的钢厂为大气氟污染的点源。在研究区内选6个取样点,分别取黄鼠大腿骨骨样、植物样和土样。 黄鼠大腿骨骨灰、植物和土壤的含氟量是随与污染源的距离和方向的不同而变化的,离污染源愈远各样品的含氟量愈低。污染源西北方向,靠近污染源的取样点污染特别严重。但是,黄鼠体重与其大腿骨骨灰含氟量间没有明显相关。黄鼠可认为是对氟污染的“耐干扰种”。 在研究区内,氟污染对植物群落的种类、生物量和群落的多样性没有明显地影响。大腿骨骨灰和植物含氟量间存在一定的回归关系,其关系式为Y=27.16X~1.02。     

宁夏引黄灌区春小麦的生态条件分析及其改善途径

本文系统分析了影响宁夏引黄灌区春小麦生产的生态条件,从作物品种、黄河肥水、土壤肥力与盐渍化、气候等方面分析了小麦与生态环境的关系,提出小麦与生态环境的平衡失调是限制灌区小麦生产潜力的关键问题,对最隹施用化肥量、合理灌溉定额及改善小麦生态环境、实现高产稳产等进行了探讨。     

畜群发展系统仿真模型的建立——黑龙江省奶牛业发展方案的研究

笔者在Lewis—Leslie结模型构的基础上,结合系统动力学思想方法,提出了分块矩阵模型。该模型除了可以研究种群结构外,还可以挂接各种投入产出信息,把生态结构模型发展成生态经济模型。本文用此模型对黑龙江省奶牛业的发展做系统仿真,提出了不同阶段的方案。     

弄岗北热带喀斯特季节性雨林15hm2动态监测样地树木死亡特征分析

以广西弄岗北热带喀斯特季节性雨林15 hm²森林动态监测样地为对象,结合2011年和2016年两次调查数据,分析5年间样地树木死亡个体的数量、径级结构和空间格局特征等。结果显示:2011年至2016年,样地有86.5%的树种出现了个体死亡的现象,死亡个体占个体总数的14.4%;死亡个体的聚集程度随空间尺度的增大而逐渐减弱;小径级个体死亡与周边邻体和环境的关联性较大;竞争是影响弄岗北热带喀斯特季节性云林树木死亡的主要因素。综合来看,北热带喀斯特季节性雨林内树木死亡并非是一个完全随机的过程,而是树木本身特征和生物与非生物环境共同作用的结果。