长白山针阔混交林不同演替阶段群落系统发育和功能性状结构

群落构建一直是生态学研究的热点,基于系统发育和功能性状量化生境过滤、竞争排斥以及随机过程在群落构建中的作用,能够深入理解群落构建机制。本研究以长白山针阔混交林不同演替阶段的3个5.2 hm~2样地(次生杨桦林、次生针阔混交林、原始椴树红松林)为平台,基于被子植物分类系统Ⅲ(Angiosperm Classification System,APGⅢ)构建的系统发育树和7个关键功能性状(叶面积、比叶面积、叶片厚度、叶片氮含量、叶片磷含量、氮磷比、最大树高),结合环境数据,分析不同演替阶段群落系统发育和功能性状结构。研究表明:(1)各演替阶段7个植物功能性状都表现出显著的系统发育信号,表明植物功能性状受系统发育历史影响;(2)系统发育和功能性状结构在不同演替阶段和不同径级均为非随机状态。随着演替的推进群落系统发育和功能性状结构由聚集走向发散;随着径级的增加,系统发育和功能性状结构的聚集程度减小,表明随着演替阶段的进行和径级增大,竞争性排斥的作用逐渐明显;(3)各演替阶段系统发育和功能性状的周转都为非随机且不同因子对两者的解释力度存在差异。演替早期空间距离的解释力度小于环境距离,说明生境过滤在群落构建中的重要性,而在演替后期空间距离的解释力度大于环境距离,验证了扩散限制在群落构建中的重要性。     

Modulation of the immune response by Middle East respiratory syndrome coronavirus

Coronavirus (CoV) infections are commonly associated with respiratory and enteric disease in humans and animals. In 2012, a new human disease called Middle East respiratory syndrome (MERS) emerged in the Middle East. MERS was caused by a virus that was originally called human coronavirus-Erasmus Medical Center/2012 but was later renamed as Middle East respiratory syndrome coronavirus (MERS-CoV). MERS-CoV causes high fever, cough, acute respiratory tract infection, and multiorgan dysfunction that may eventually lead to the death of the infected individuals. The exact origin of MERS-CoV remains unknown, but the transmission pattern and evidence from virological studies suggest that dromedary camels are the major reservoir host, from which human infections may sporadically occur through the zoonotic transmission. Human to human transmission also occurs in healthcare facilities and communities. Recent studies on Middle Eastern respiratory continue to highlight the need for further understanding the virus-host interactions that govern disease severity and infection outcome. In this review, we have highlighted the major mechanisms of immune evasion strategies of MERS-CoV. We have demonstrated that M, 4a, 4b proteins and Plppro of MERS-CoV inhibit the type I interferon (IFN) and nuclear factor-κB signaling pathways and therefore facilitate innate immune evasion. In addition, nonstructural protein 4a (NSP4a), NSP4b, and NSP15 inhibit double-stranded RNA sensors. Therefore, the mentioned proteins limit early induction of IFN and cause rapid apoptosis of macrophages. MERS-CoV strongly inhibits the activation of T cells with downregulation of antigen presentation. In addition, uncontrolled secretion of interferon ɣ-induced protein 10 and monocyte chemoattractant protein-1 can suppress proliferation of human myeloid progenitor cells.     

funrar: An R package to characterize functional rarity

Emphasis has been put in recent ecological research on investigating phylogenetic, functional and taxonomic facets of biological diversity. While a flourishing number of indices have been proposed for assessing functional diversity, surprisingly few options are available to characterize functional rarity. Functional rarity can play a key role in community and ecosystem dynamics. We introduce here the funrar R package to quantify functional rarity based on species trait differences and species frequencies at local and regional scales. Because of the increasing availability of big datasets in macroecology and biogeography, we optimized funrar to work with large datasets of thousands of species and sites. We illustrate the use of the package to investigate the functional rarity of North and Central American mammals.     

IL17A augments autophagy in Mycobacterium tuberculosis-infected monocytes from patients with active tuberculosis in association with the severity of the disease

During mycobacterial infection, macroautophagy/autophagy, a process modulated by cytokines, is essential for mounting successful host responses. Autophagy collaborates with human immune responses against Mycobacterium tuberculosis (Mt) in association with specific IFNG secreted against the pathogen. However, IFNG alone is not sufficient to the complete bacterial eradication, and other cytokines might be required. Actually, induction of Th1 and Th17 immune responses are required for protection against Mt. Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity. Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1. Patients with active disease were classified as high responder (HR) or low responder (LR) according to their T cell responses against Mt. IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response. In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients. Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction. Therefore, in severe tuberculosis patients' monocytes, IL17A was unable to augment autophagy because of a defect in the MAPK1/3 signaling pathway. In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing. Our findings might contribute to recognize new targets for the development of novel therapeutic tools to fight the pathogen.