渗透胁迫对高粱根中K~+累积的刺激作用

本工作中发现,2,4—二硝基酚(DNP)可有效地洗去高粱根中的K~+,从而提高了测定和比较K~+累积量的显示度和准确性,渗透胁迫下,高粱根中K~+的累积量比对照增加高达6.7倍;同时,组织的H~+分泌明显受到促进,动力学研究表明,经PEG胁迫的高粱根对K~+的亲和力显著增强。对照:K_m=9.25mmol/L,V_m=23.6μmolg~(-1)DW min~(-1);PEG处理者:K_m=27.25μmol/L,V_m=14.71μmolg~(-1)DW min~(-1).地上部的存在有利于 K~+的吸收。渗透胁迫所促进的K~+吸收可被亚胺环己酮(CHM)完全抑制,这一结果暗示渗透胁迫诱导的K~+吸收的增加依赖于蛋白质的诱导合成,本文讨论了K~+吸收增强的可能机理。     

Ribosomal protein L22-like1 promotes prostate cancer progression by activating PI3K/Akt/mTOR signalling pathway

Prostate cancer (PCa) is one of the most common malignancies in men. Ribosomal protein L22-like1 (RPL22L1), a component of the ribosomal 60 S subunit, is associated with cancer progression, but the role and potential mechanism of RPL22L1 in PCa remain unclear. The aim of this study was to investigate the role of RPL22L1 in PCa progression and the mechanisms involved. Bioinformatics and immunohistochemistry analysis showed that the expression of RPL22L1 was significantly higher in PCa tissues than in normal prostate tissues. The cell function analysis revealed that RPL22L1 significantly promoted the proliferation, migration and invasion of PCa cells. The data of xenograft tumour assay suggested that the low expression of RPL22L1 inhibited the growth and invasion of PCa cells in vivo. Mechanistically, the results of Western blot proved that RPL22L1 activated PI3K/Akt/mTOR pathway in PCa cells. Additionally, LY294002, an inhibitor of PI3K/Akt pathway, was used to block this pathway. The results showed that LY294002 remarkably abrogated the oncogenic effect of RPL22L1 on PCa cell proliferation and invasion. Taken together, our study demonstrated that RPL22L1 is a key gene in PCa progression and promotes PCa cell proliferation and invasion via PI3K/Akt/mTOR pathway, thus potentially providing a new target for PCa therapy.     

生长抑素受体2的小鼠时空组织表达谱

生长抑素(somatostatin, SST)作为一种抑制性多肽激素,在多种生物过程中发挥重要的功能。生长抑素受体2 (somatostatin receptor 2, SSTR2)作为生长抑素表达最广泛的受体在多种组织中表达,但其表达的具体细胞类型尚不清楚。本研究在小鼠不同发育阶段的多种组织中鉴定了SSTR2蛋白表达的细胞类型。通过多色免疫荧光在小鼠胚胎期15.5 d、出生后1 d、7 d、15 d、3个月和6个月的脑、骨、肺、肠道、皮肤、胃、脾和肾等组织中检测了Sstr2基因的表达。结果发现Sstr2在不同发育阶段的多种组织的特定细胞类型中表达,包括脑神经元和星形胶质细胞,骨的间充质基质细胞、造血细胞和B细胞,肺的巨噬细胞、Ⅱ型肺泡上皮细胞和气道纤毛细胞,肠道的上皮细胞和神经元,皮肤的毛囊细胞,胃体的上皮细胞,脾的造血干细胞、造血祖细胞和神经纤维,肾的肾小管上皮细胞等。本研究确定了小鼠多组织不同发育阶段Sstr2表达的细胞类型,为生长抑素与生长抑素受体2的生理功能研究提供了新的线索。     

基于转录组测序的宁夏枸杞不同品种果实活性成分合成差异表达基因分析

为探究不同品种宁夏枸杞果实活性成分生物合成相关基因的表达水平,筛选关键差异表达基因(differentially expressed genes,DEGs),揭示宁夏枸杞品种间活性成分含量差异的分子机制,本研究采用Illumina NovaSeq 6000高通量测序技术,对宁夏枸杞‘宁杞1号’和‘宁杞7号’青果期、转色期及成熟期果实进行转录组测序,比较2个品种果实不同发育期相关基因表达谱的变化。结果显示:转录组测序共获得811818178条clean reads,有121.76 Gb有效数据。‘宁杞1号’和‘宁杞7号’在青果期、转色期和成熟期差异表达基因分别有2827、2552和2311个;分别有2153、2050和1825个差异基因在基因本体论(gene ontology,GO)、京都基因与基因组百科全书(Kyoto encyclopedia of genes and genomes,KEGG)富集分析和同源蛋白簇(clusters of orthologous groups of proteins,KOG)分析等6个数据库中被成功注释。青果期、转色期和成熟期果实的差异表达基因,在GO数据库分别有1307、865和624个被富集到生物学过程、细胞组分及分子功能3个部分中;KEGG通路富集结果均集中在代谢途径、次生代谢物生物合成和植物-病原互作过程;在KOG数据库,3个发育期分别注释了1775、1751和1541个差异表达基因。对注释的基因进行PubMed数据库检索,在青果期、转色期和成熟期分别筛选到与枸杞活性成分合成相关的差异表达基因18、26和24个,这些基因主要参与类胡萝卜素、类黄酮、萜类、生物碱和维生素等代谢途径。选取7个差异表达基因进行RT-qPCR验证,结果与转录组测序数据表达趋势一致。本研究从转录水平为不同品种宁夏枸杞活性成分含量差异提供了初步证据,为进一步挖掘枸杞活性成分生物合成的关键基因及解析其表达调控机制提供了研究基础。     

评论：塑料结合模块促进聚对苯二甲酸乙二醇酯的酶法降解

塑料的大量生产和无节制的使用已造成严重的环境污染。为了减少塑料废物对环境的影响,近年来塑料酶法降解已成为国内外研究者关注的热点。例如,通过蛋白质工程策略提高塑料降解酶催化活性和热稳定性,进一步提高酶法降解的效率。另外,通过融合酶策略将塑料结合模块与塑料降解酶融合,也可以促进塑料降解。近期发表在期刊Chem Catalysis的一项研究表明,采用碳水化合物结合模块融合策略可以在低浓度(<10 wt%)的底物聚对苯二甲酸乙二醇酯[poly(ethylene terephthalate),PET]中提高塑料降解酶的活性。但是在高浓度底物(10 wt%−20 wt%)中,该策略无法提高PET的酶法降解。该项研究对于采用塑料结合模块促进酶法降解塑料具有重要的指导意义。     

Investigations of interaction mechanism and conformational variation of serum albumin affected by artemisinin and dihydroartemisinin

In this work, binding interactions of artemisinin (ART) and dihydroartemisinin (DHA) with human serum albumin (HSA) and bovine serum albumin (BSA) were investigated thoroughly to illustrate the conformational variation of serum albumin. Experimental results indicated that ART and DHA bound strongly with the site I of serum albumins via hydrogen bond (H-bond) and van der Waals force and subsequently statically quenched the intrinsic fluorescence of serum albumins through concentration-dependent manner. The quenching abilities of two drugs on the intrinsic fluorescence of HSA were much higher than the quenching abilities of two drugs on the intrinsic fluorescence of BSA. Both ART and DHA, especially DHA, caused the conformational variation of serum albumins and reduced the α-helix structure content of serum albumins. DHA with hydrophilic hydroxyl group bound with HSA more strongly, suggesting the important roles of the chemical polarity and the hydrophilicity during the binding interactions of two drugs with serum albumins. These results reveal the molecular understanding of binding interactions between ART derivatives and serum albumins, providing vital information for the future application of ART derivatives in biological and clinical areas.     

论Paracarinachitids

研究证明Paracarinachitids的外骨骼都不是由8个骨板组成,骨片具有清楚的微层构造,表明它们是由叠覆的生长层组成,每个生长节上有一个小刺,在顶端下侧面前端都有肾形缺凹。同一标本上存在顶端部的融合和远顶端部的分节彼此递交的现象表明这种表象上的差异是后期次生磷灰石包裹或腐蚀的结果;其下侧缘融合和下侧面无缝隙的现象说明将Paracarinachites spinus的骨片分成头板、中间板和尾板是没有根据的。骨片表面存在的针状体是成岩作用的产物,它是粘土矿物和磷酸盐针状结晶体而不是多板纲的骨针。凡此强有力地说明Yangtzechiton是Paracarinachites的晚出同义名。根据形态功能、组织结构,特别是叠覆状排列的骨片和孤立的生长节等特征,paracarinachitids 可能与zhijinitids有密切关系,但两者是否同源尚缺少进一步的证据、据此,笔者认为将paracarinachitids 暂置于分类位置未定的具骨片后生动物较妥。     

外显子与内含子序列分维的双碱基研究

引入碱基间的关联,研究了外显子和内含子序列以双碱基为单位的分维,我们发现在这种情况下,外显子和内显子序列在短程和中程存在自相似性并分别定义了这两个区域的分维。结果表明,短程的分维值Ｄｇ一般比中程的Ｄｍ大,外显子的两个分维值比内含子大。我们改变双联体的位相而分维却不变,这反映出在双联体基础上,外显子的不规则性大于内含子,短程的不规则性大于中程,外显子和内含子序列对以２为周期的结构没有位相的特异性。     

TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation

Nonalcoholic fatty liver disease (NAFLD) is a strong stimulant of cardiovascular diseases, affecting one-quarter of the world's population. TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia–reperfusion injury; however, its effect on NAFLD/nonalcoholic steatohepatitis (NASH) has not been reported. In this study, we demonstrated that TBC1D25 expression is upregulated in NASH. TBC1D25 deficiency aggravated hepatic steatosis, inflammation, and fibrosis in NASH. In vitro tests revealed that TBC1D25 overexpression restrained NASH responses. Subsequent mechanistic validation experiments demonstrated that TBC1D25 interfered with NASH progression by inhibiting abnormal lipid accumulation and inflammation. TBC1D25 deficiency significantly promoted NASH occurrence and development. Therefore, TBC1D25 may potentially be used as a clinical therapeutic target for NASH treatment.