磷酸肌醇激酶FAB1调控拟南芥根毛伸长

FAB1/PIKfyve是介导PI(3,5)P₂ (磷脂酰肌醇3,5-二磷酸)生物合成的磷酸肌醇激酶。在动物和酵母(Saccharomyces cerevisiae)中, PI(3,5)P₂参与调控胞内膜运输, 但在植物中的研究较少。该文通过分析拟南芥(Arabidopsis thaliana) FAB1的T-DNA插入突变体的表型解析PI(3,5)P₂的生物学功能。拟南芥FAB1基因家族包含FAB1A、FAB1B、FAB1C和FAB1D四个基因。研究发现, fab1a/b呈现雄配子体致死的表型。利用遗传杂交获得fab1b/c/d三突变体, 发现FAB1B、FAB1C和FAB1D功能缺失导致根毛相比野生型变短, 经FAB1特异性抑制剂YM201636处理后的野生型中也观察到相似的短根毛表型。此外, fab1b/c/d三突变体中DR5转录水平降低。同时, 外源施加生长素类似物2,4-D和NAA能部分恢复fab1b/c/d植株短根毛的表型, 但fab1b/c/d突变体对生长素转运抑制剂(1-NOA和TIBA)的敏感性与野生型相似。此外, FAB1B/C/D功能缺失使根毛中ROS的含量减少且影响肌动蛋白的表达。上述结果表明, FAB1B/C/D通过调控生长素分布、ROS含量和肌动蛋白的表达影响拟南芥根毛伸长。     

金银花花形基因的发掘及生物信息学分析

金银花作为我国重要的中药材,具有消炎、抗菌、抗病毒、抗氧化、防癌等多种功效。随着金银花市场供需矛盾日益加剧,通过分子标记辅助选择育种方法来培育高产优质品种势在必行。通过NCBI的Blast工具扫描金银花蛋白组数据发掘花形候选基因,并执行候选基因的亲缘关系分析、结构域分析、表达模式分析、理化性质分析、蛋白质结构预测等一系列生物信息学分析。依据拟南芥调控花形的ABE类基因,通过NCBI-Blast工具扫描金银花氨基酸序列,筛选出包含MADS结构域的8个调控花形的金银花候选基因。经LjaFGD表达模式分析发现,金银花的花中GWHGAAZE016592和GWHGAAZE014905表达量显著高于其他部位,可能正向调控金银花花形。GWHGAAZE014905是一个包含MADS结构域的调控花器官发育的B类基因;GWHGAAZE016592是AP3同源基因。生物信息学分析发现,GWHGAAZE016592和GWHGAAZE014905均是稳定的亲水蛋白,属于非分泌蛋白,包括Motif1、Motif3、Motif4、Motif2、Motif6和Motif5,蛋白质三级结构模板为6byy.2.A和4ox0.2.C。GWHGAAZE014905被定位到细胞核上,而GWHGAAZE016592被定位到叶绿体上,且包含1个位于151~173 bp的跨膜螺旋区域,属于膜蛋白。研究结果为分子标记辅助选择方式培育道地高产优质金银花品种提供了基因资源和分子标记。     

Land masses and oceanic currents drive population structure of Heritiera littoralis,a widespread mangrove in the Indo‐West Pacific

Phylogeographic forces driving evolution of sea‐dispersed plants are often influenced by regional and species characteristics, although not yet deciphered at a large spatial scale for many taxa like the mangrove species Heritiera littoralis. This study aimed to assess geographic distribution of genetic variation of this widespread mangrove in the Indo‐West Pacific region and identify the phylogeographic factors influencing its present‐day distribution. Analysis of five chloroplast DNA fragments’ sequences from 37 populations revealed low genetic diversity at the population level and strong genetic structure of H. littoralis in this region. The estimated divergence times between the major genetic lineages indicated that glacial level changes during the Pleistocene epoch induced strong genetic differentiation across the Indian and Pacific Oceans. In comparison to the strong genetic break imposed by the Sunda Shelf toward splitting the lineages of the Indian and Pacific Oceans, the genetic differentiation between Indo‐Malesia and Australasia was not so prominent. Long‐distance dispersal ability of H. littoralis propagules helped the species to attain transoceanic distribution not only across South East Asia and Australia, but also across the Indian Ocean to East Africa. However, oceanic circulation pattern in the South China Sea was found to act as a barrier creating further intraoceanic genetic differentiation. Overall, phylogeographic analysis in this study revealed that glacial vicariance had profound influence on population differentiation in H. littoralis and caused low genetic diversity except for the refugia populations near the equator which might have persisted through glacial maxima. With increasing loss of suitable habitats due to anthropogenic activities, these findings therefore emphasize the urgent need for conservation actions for all populations throughout the distribution range of H. littoralis.     

Long non-coding RNA LINC00488 facilitates thyroid cancer cell progression through miR-376a-3p/PON2

Objective: Long non-coding RNAs (lncRNAs) recently have been identified as influential indicators in a variety of malignancies. The aim of the present study was to identify a functional lncRNA LINC00488 and its effects on thyroid cancer in the view of cell proliferation and apoptosis.Methods: In order to evaluate the effects of LINC00488 on the cellular process of thyroid cancer, we performed a series of in vitro experiments, including cell counting kit-8 (CCK-8) assay, EdU (5-ethynyl-2′-deoxyuridine) assay, flow cytometry, transwell chamber assay, Western blot and RT-qPCR. The target gene of LINC00488 was then identified by bioinformatics analysis (DIANA and TargetScan). Finally, a series of rescue experiments was conducted to validate the effect of LINC00488 and its target genes on proliferation, migration, invasion and apoptosis of thyroid cancer.Results: Our findings revealed that LINC00488 was highly expressed in thyroid cancer cell lines (BCPAP, BHP5-16, TPC-1 and CGTH-W3) and promoted the proliferation, migration and invasion, while inhibited the apoptosis of thyroid cancer cells (BCPAP and TPC-1). The results of bioinformatics analysis and dual luciferase reporter gene assay showed that LINC00488 could directly bind to miR-376a-3p and down-regulated the expression level of miR-376a-3p. In addition, Paraoxonase-2 (PON2) was a target gene of miR-376a-3p and negatively regulated by miR-376a-3p. Rescue experiment indicated that LINC00488 might enhance PON2 expression by sponging miR-376a-3p in thyroid cancer.Conclusion: Taken together, our study revealed that lncRNA LINC00488 acted as an oncogenic gene in the progression of thyroid cancer via regulating miR-376a-3p/PON2 axis, which indicated that LINC00488-miR-376a-3p-PON2 axis could serve as novel biomarkers or potential targets for the treatment of thyroid cancer.     

Integrative hormone and transcriptome analysis underline the role of abscisic acid in seed shattering of weedy rice

Plant Growth Regulation - Weedy rice is one of the most severe weeds in paddy fields, characterized by its high degree of seed shattering. Abscisic acid (ABA) serves as an abscission-accelerating...     

FIT2 organizes lipid droplet biogenesis with ER tubule-forming proteins and septins

Lipid droplets (LDs) are critical for lipid storage and energy metabolism. LDs form in the endoplasmic reticulum (ER). However, the molecular basis for LD biogenesis remains elusive. Here, we show that fat storage–inducing transmembrane protein 2 (FIT2) interacts with ER tubule-forming proteins Rtn4 and REEP5. The association is mainly transmembrane domain based and stimulated by oleic acid. Depletion of ER tubule-forming proteins decreases the number and size of LDs in cells and Caenorhabditis elegans, mimicking loss of FIT2. Through cytosolic loops, FIT2 binds to cytoskeletal protein septin 7, an interaction that is also required for normal LD biogenesis. Depletion of ER tubule-forming proteins or septins delays nascent LD formation. In addition, FIT2-interacting proteins are up-regulated during adipocyte differentiation, and ER tubule-forming proteins, septin 7, and FIT2 are transiently enriched at LD formation sites. Thus, FIT2-mediated nascent LD biogenesis is facilitated by ER tubule-forming proteins and septins.     

Interactions between commensal bacteria and viral infection: insights for viral disease control in farmed animals

Viral diseases cause serious economic loss in farmed animals industry. However, the efficacy of remedies for viral infection in farmed animals is limited, and treatment strategies are generally lacking for aquatic animals. Interactions of commensal microbiota and viral infection have been studied in recent years, demonstrating a third player in the interaction between hosts and viruses. Here, we discuss recent developments in the research of interactions between commensal bacteria and viral infection,including both promotion and inhibition effect of commensal bacteria on viral pathogenesis, as well as the impact of viral infection on commensal microbiota. The antiviral effect of commensal bacteria is mostly achieved through priming or regulation of the host immune responses, involving differential microbial components and host signaling pathways, and gives rise to various antiviral probiotics. Moreover, we summarize studies related to the interaction between commensal bacteria and viral infection in farmed animals, including pigs, chickens, fish and invertebrate species. Further studies in this area will deepen our understanding of antiviral immunity of farmed animals in the context of commensal microbiota, and promote the development of novel strategies for treatment of viral diseases in farmed animals.     

Pre-induced adult human peripheral blood mononuclear cells migrate widely into the degenerative retinas of rd1 mice

Background aimsRecent advances in stem cell research have raised the possibility of stem cells repairing or replacing retinal photoreceptor cells that are either dysfunctional or lost in many retinal diseases. Various types of stem cells have been used to replace retinal photoreceptor cells. Recently, peripheral blood stem cells, a small proportion of pluripotent stem cells, have been reported to mainly exist in the peripheral blood mononuclear cells (PBMCs).MethodsIn this study, the effects of pre-induced adult human PBMCs (hPBMCs) on the degenerative retinas of rd1 mice were investigated. Freshly isolated adult hPBMCs were pre-induced with the use of the conditioned medium of rat retinas for 4 days and were then labeled with chloromethyl-benzamidodialkylcarbocyanine (CM-DiI) and then transplanted into the subretinal space of the right eye of rd1 mice through a trans-scleral approach. The right eyes were collected 30 days after transplantation. The survival and migration of the transplanted cells in host retinas were investigated by whole-mount retinas, retinal frozen sections and immunofluorescent staining.ResultsAfter subretinal transplantation, pre-induced hPBMCs were able to survive and widely migrate into the retinas of rd1 mice. A few CM-DiI–labeled cells migrated into the inner nuclear layer and the retinal ganglion cell layer. Some transplanted cells in the subretinal space of rd1 host mice expressed the human photoreceptor–specific marker rhodopsin.ConclusionsThis study suggests that pre-induced hPBMCs may be a potential cell source of cell replacement therapy for retinal degenerative diseases.     

Detection and Validation of Circulating Endothelial Cells,a Blood-based Diagnostic Marker of Acute Myocardial Infarction

Background

Circulating endothelial cells (CECs) are markers of vascular damage that have clinical relevance in many diseases, including acute myocardial infarction (AMI), and may be predictors of treatment responses. Herein, we investigated the diagnostic and prognostic value of CEC monitoring in AMI patients and a murine model.

Methodology/Principal Findings

CECs were defined as Hoechst 33342⁺/CD45^−/CD31⁺/CD146⁺/CD133⁻ in human blood samples and Hoechst 33342⁺/CD45^−/CD31⁺/KDR⁺/CD117⁻ in murine samples. To evaluate the validity and variability of our CEC detection system, peripheral blood samples of vascular endothelial growth factor-treated athymic nude mice and AMI patients were collected and subjected to intra-assay analysis. CEC detection by flow cytometry and real-time PCR were compared. Blood samples were obtained from 61 AMI patients, 45 healthy volunteers and 19 samples of the original AMI patients accepted one month treatment, via flow cytometry and expressed as a percentage of peripheral blood mononuclear cells.

Results

Our CEC detection method was validated and had limited variability. CEC concentrations were higher in AMI patients compared to healthy controls. One month post-treatment, CECs levels decreased significantly.

Conclusions/Significance

CEC levels may be useful as a diagnostic and prognostic biomarker in AMI patients.