TRIM37 prevents formation of condensate-organized ectopic spindle poles to ensure mitotic fidelity

Centrosomes are composed of a centriolar core surrounded by pericentriolar material that nucleates microtubules. The ubiquitin ligase TRIM37 localizes to centrosomes, but its centrosomal roles are not yet defined. We show that TRIM37 does not control centriole duplication, structure, or the ability of centrioles to form cilia but instead prevents assembly of an ectopic centrobin-scaffolded structured condensate that forms by budding off of centrosomes. In ∼25% of TRIM37-deficient cells, the condensate organizes an ectopic spindle pole, recruiting other centrosomal proteins and acquiring microtubule nucleation capacity during mitotic entry. Ectopic spindle pole–associated transient multipolarity and multipolar segregation in TRIM37-deficient cells are suppressed by removing centrobin, which interacts with and is ubiquitinated by TRIM37. Thus, TRIM37 ensures accurate chromosome segregation by preventing the formation of centrobin-scaffolded condensates that organize ectopic spindle poles. Mutations in TRIM37 cause the disorder mulibrey nanism, and patient-derived cells harbor centrobin condensate-organized ectopic poles, leading us to propose that chromosome missegregation is a pathological mechanism in this disorder.     

MicroRNA-137-3p Protects PC12 Cells Against Oxidative Stress by Downregulation of Calpain-2 and nNOS

The imbalance between excess reactive oxygen species (ROS) generation and insufficient antioxidant defenses contribute to a range of neurodegenerative diseases. High ROS levels damage cellular macromolecules such as DNA, proteins and lipids, leading to neuron vulnerability and eventual death. However, the underlying molecular mechanism of the ROS regulation is not fully elucidated. Recently, an increasing number of studies suggest that microRNAs (miRNAs) emerge as the targets in regulating oxidative stress. We recently reported the neuroprotective effect of miR-137-3p for brachial plexus avulsion-induced motoneuron death. The present study is sought to investigate whether miR-137-3p also could protect PC12 cells against hydrogen peroxide (H₂O₂) induced neurotoxicity. By using cell viability assay, ROS assay, gene and protein expression assay, we found that PC-12 cells exposed to H₂O₂ exhibited decreased cell viability, increased expression levels of calpain-2 and neuronal nitric oxide synthase (nNOS), whereas a decreased miR-137-3p expression. Importantly, restoring the miR-137-3p levels in H₂O₂ exposure robustly inhibited the elevated nNOS, calpain-2 and ROS expression levels, which subsequently improved the cell viability. Furthermore, the suppressive effect of miR-137-3p on the elevated ROS level under oxidative stress was considerably blunted when we mutated the binding site of calpain-2 targted by miR-137-3p, suggesting the critical role of calpain-2 involving the neuroprotective effect of miR-137-3p. Collectively, these findings highlight the neuroprotective role of miR-137-3p through down-regulating calpain and NOS activity, suggesting its potential role for combating oxidative stress insults in the neurodegenerative diseases.

     

中国鹿角兰属(兰科)植物新资料

报道了中国兰科(Orchidaceae)鹿角兰属(Pomatocalpa)一新记录种——纹瓣鹿角兰［P. tonkinense (Gagnep.) Seidenf.］,凭证标本保存于广西植物研究所标本馆(IBK)。纹瓣鹿角兰的花序疏生多数花,萼片、花瓣均具2条紫色条纹,中萼片及花瓣远长于侧萼片,与中国原记录的2种鹿角属植物容易区分。该研究提供了新记录种的形态描述、中国鹿角兰属植物图版及分种检索表。     

江西省2010年柯萨奇病毒A组24型变异株的全基因组序列分析

急性出血性结膜炎(Acute hemorrhagic conjunctivitis,AHC)是目前人类最常见的眼病之一,柯萨奇病毒A组24型变异株(Coxsackievirus A24 variant,CV-A24v)是近年来报道引起该病的主要病原体。本研究选取10株来自江西省2010年AHC暴发疫情的CV-A24v,采用特异性引物扩增并测定其全基因组序列。对该10条CV-A24v的全基因组序列进行系统发育分析以及重组分析,计算本研究测定的江西10条以及GenBank中所有22条CV-A24v的全基因组序列的氨基酸置换熵值,并预测其正向选择位点。结果表明,在江西10条CV-A24v基因组序列中未检测到重组。基于全基因组序列构建的最大似然树表明江西10株CV-A24v属于GIV基因型,且分处于两条传播链。对上述32条CV-A24v序列的氨基酸置换熵值计算,共得到25个易突变位点(熵值>0.6),易突变概率最高的区段为2A区。基于Datamonkey中FUBAR和FEL模型分析,发现位于结构蛋白VP2区的234位氨基酸为两种模型共同获得的CV-A24v的正向选择位点。本研究分析了江西10株CV-A24v的全基因组序列特征,为CV-A24v引起的AHC防控工作提供了基础资料。