北京唇形科一新记录属——龙头草属

该文报道了发现于北京市密云区的1种被子植物新记录——荨麻叶龙头草[Meehania urticifolia(Miq.)Makino],其所隶属的龙头草属(Meehania Britton)为北京分布新记录。描述了荨麻叶龙头草的形态特征与生境,凭证标本藏于浙江大学标本馆(HZU)。荨麻叶龙头草于1899年首次发现于日本,是东北亚分布植物,此前在中国仅分布于东北。北京云蒙山发现的分布点,显然是该种目前在中国分布最西的分布点,可能于冰川期从东北亚迁移而来。     

中国环缘蝽属昆虫记述(半翅目:姬缘蝽科)

环缘蝽属(Stictopleurus Stal)建立于1872年,为半翅目(Hemiptera)姬缘蝽科(Rhopalidae)中的一个类群。Reuter(1885)将其降为姬缘蝽属(Corizus Fallen)的一个亚属,该意见曾被一些学者所采纳,如Puton(1886/1899),Ragusa(1907),Van Duzee(1916),Torre-Bueno(1914)等;Muzik(1904)亦曾将其作为伊缘蝽属(Rhopalus Schil-ling)的一个亚属;但后来多数学者及近代的分类学工作者均将其视为一个独立的属,如Oshanin(1906/1912),De Seabra(1927),Harris(1943),Chopra(1967),Gollner-     

口岸检疫性蚧类害虫疫情截获分析

【目的】了解我国口岸截获的检疫性蚧类害虫情况,为口岸进一步做好植物检疫工作提供参考。【方法】收集整理2010—2019年口岸截获蚧类害虫数据,重点统计分析被截获蚧类害虫种类、时间、数量、寄主、来源地的变化和关系。【结果】2010—2019年,我国各口岸共截获检疫性蚧类害虫24541种次,年截获种次总体呈上升的趋势。截获检疫性蚧类害虫共有12种,截获频率最高的3种为无花果蜡蚧、松突圆蚧和扶桑绵粉蚧。截获该类害虫数量最多的3个关区为深圳关、南宁关和上海关。货物检疫为主要截获途径,主要截获寄主植物为榴梿、香蕉、红毛丹、番荔枝。截获货物来源地为除南极洲以外六大洲的49个国家或地区,其中尤以东南亚为主,代表国家包括泰国、越南和菲律宾。【结论】蚧类害虫的截获与进口水果贸易密切相关,在相关贸易量不断增加的背景下,应警惕蚧类害虫疫情持续传入我国的风险,建议有关部门进一步完善检疫管理体系,提升检测和监测技术水平,加强检疫处置能力。     

人上皮细胞角蛋白纤维结构转化的分析

用0℃冷冻处理2—3 h,一些PcaSE-1和BEL-7404细胞的角蛋白纤维能部分地转化成凝聚颗粒,但在HeLa 和CNE 细胞中不发生这种角蛋白纤维结构转化。当回复温度到37℃15—30 min 时,PcaSE-1 和BEL-7404细胞的这种结构转化能快速回复。相反,在HeLa 和CNE 细胞有丝分裂时,角蛋白纤维能转化成凝聚颗粒,但PcaSE-1细胞和BEL-7404细胞的角蛋白纤维网始终维持纤维状态,且围绕纺锤体分布。上述结果表明:两类上皮细胞角蛋白纤维结构的转化似由不同因子所引起。我们的结果还指出:(1)单用秋水仙素或用秋水仙素和细胞松弛素D 合并处理PcaSE-1细胞不能引起角蛋白纤维凝聚。但经秋水仙素解聚微管后,会增强细胞对冷处理的凝聚反应。(2)冷处理时角蛋白纤维凝聚的形成与细胞是否具有两套不同的中间纤维无关。(3)予先用TritonX-100抽提细胞,角蛋白纤维在冷冻后不能转化成凝聚颗粒。(4)冷冻处理引起的结构转化可能是某些上皮细胞系的角蛋白纤维的一种特殊性质。     

利用原生质体融合技术选育防治植物病虫害的基因重组菌株

本试验选用抗菌蛋白产生菌枯草芽孢杆菌(B.subtilis) TG26和晶体蛋白产生菌苏云金芽孢杆菌(B.thuringiesis subsp,pacifeus) AS1.904的营养缺陷型衍生株,在聚乙二醇的诱导下进行原生质体种间融合,获得了表现双亲遗传性状的种间融合菌株。融合率为7.52×10~6,融合子经传代10次,稳定率为19.5%。融合菌株的菌落和细胞形态与亲本株明显不同。通过SDS-聚丙烯酰胺凝胶电泳检测,融合菌株表达了亲本的抗菌蛋白和毒素蛋白。抑菌杀虫试验表明,融合重组菌株具有抑制多种植物病原菌和毒杀鳞翅目幼虫的能力。     

Development and validation of robust metabolism-related gene signature in the prognostic prediction of hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is one of the most common malignant tumours worldwide. Given metabolic reprogramming in tumours was a crucial hallmark, several studies have demonstrated its value in the diagnostics and surveillance of malignant tumours. The present study aimed to identify a cluster of metabolism-related genes to construct a prediction model for the prognosis of HCC. Multiple cohorts of HCC cases (466 cases) from public datasets were included in the present analysis. (GEO cohort) After identifying a list of metabolism-related genes associated with prognosis, a risk score based on metabolism-related genes was formulated via the LASSO-Cox and LASSO-pcvl algorithms. According to the risk score, patients were stratified into low- and high-risk groups, and further analysis and validation were accordingly conducted. The results revealed that high-risk patients had a significantly worse 5-year overall survival (OS) than low-risk patients in the GEO cohort. (30.0% vs. 57.8%; hazard ratio [HR], 0.411; 95% confidence interval [95% CI], 0.302–0.651; p < 0.001) This observation was confirmed in the external TCGA-LIHC cohort. (34.5% vs. 54.4%; HR 0.452; 95% CI, 0.299–0.681; p < 0.001) To promote the predictive ability of the model, risk score, age, gender and tumour stage were integrated into a nomogram. According to the results of receiver operating characteristic curves and decision curves analysis, the nomogram score possessed a superior predictive ability than conventional factors, which indicate that the risk score combined with clinicopathological features was able to achieve a robust prediction for OS and improve the individualized clinical decision making of HCC patients. In conclusion, the metabolic genes related to OS were identified and developed a metabolism-based predictive model for HCC. Through a series of bioinformatics and statistical analyses, the predictive ability of the model was approved.     

Transmembrane kinase 1-mediated auxin signal regulates membrane-associated clathrin in Arabidopsis roots

Clathrin-mediated endocytosis (CME) is the major endocytic pathway in eukaryotic cells that directly regulates abundance of plasma membrane proteins. Clathrin triskelia are composed of clathrin heavy chains (CHCs) and light chains (CLCs), and the phytohormone auxin differentially regulates membrane-associated CLCs and CHCs, modulating the endocytosis and therefore the distribution of auxin efflux transporter PIN-FORMED2 (PIN2). However, the molecular mechanisms by which auxin regulates clathrin are still poorly understood. Transmembrane kinase (TMKs) family proteins are considered to contribute to auxin signaling and plant development; it remains unclear whether they are involved in PIN transport by CME. We assessed TMKs involvement in the regulation of clathrin by auxin, using genetic, pharmacological, and cytological approaches including live-cell imaging and immunofluorescence. In tmk1 mutant seedlings, auxin failed to rapidly regulate abundance of both CHC and CLC and to inhibit PIN2 endocytosis, leading to an impaired asymmetric distribution of PIN2 and therefore auxin. Furthermore, TMK3 and TMK4 were shown not to be involved in regulation of clathrin by auxin. In summary, TMK1 is essential for auxin-regulated clathrin recruitment and CME. TMK1 therefore plays a critical role in the establishment of an asymmetric distribution of PIN2 and an auxin gradient during root gravitropism.     

BmCaspase-8-like regulates autophagy by suppressing BmDREDD-mediated cleavage of BmATG6

Autophagy plays an important role in tissue remodeling during insect development. The interplay between autophagy-related (ATG) proteins and caspases regulates the autophagic activity of ATGs, thereby modulating the process of autophagy. Our previous study characterized BmCaspase-8-like (BmCasp8L) as a caspase suppressor that inhibits apoptosis and immune signaling by suppressing the activation of death-related ced-3/Nedd2-like caspase (DREDD), a caspase-8 homolog in silkworm. In this study, we explored the regulatory role of BmCasp8L in autophagy. We found that the expression of Bmcasp8l increased from the late spinning stage to the pupa stage in the posterior silk gland (PSG), correlating with the expression patterns of Bmatg8 and Bmatg6. RNA interference-mediated downregulation of BmCasp8L expression significantly decreased starvation-induced autophagic influx as determined by the levels of BmATG8–phosphatidylethanolamine and the percentage of cells displaying punctate enhanced green fluorescent protein-BmATG8. Conversely, the overexpression of BmCasp8L significantly increased autophagic influx. We also found that BmCasp8L underwent autophagic degradation induced by starvation and that it was colocalized with BmATG8. Lastly, we demonstrated that BmDREDD attenuated autophagy and BmCasp8L suppressed BmDREDD-mediated cleavage of BmATG6. Taken together, our results demonstrated that BmCasp8L is a novel proautophagic molecule which suppresses BmDREDD-mediated cleavage of BmATG6 and is a target for autophagy.