The Arabidopsis tt19-4 mutant differentially accumulates proanthocyanidin and anthocyanin through a 3' amino acid substitution in glutathione S-transferase

The Arabidopsis transparent testa (tt) mutant tt19-4 shows reduced seed coat colour, but stains darkly with DMACA and accumulates anthocyanins in aerial tissues. Positional cloning showed that tt19-4 was allelic to tt19-1 and has a G-to-T mutation in a conserved 3'-domain in the TT19-4 gene. Soluble and unextractable seed proanthocyanidins and hydrolysis of unextractable proanthocyanidin differ between wild-type Col-4 and both mutants. However, seed quercetins, unextractable proanthocyanidin hydrolysis, and seedling anthocyanin content, and flavonoid gene expression differ between tt19-1 and tt19-4. Transformation of tt19-1 with a TT19-4 cDNA results in vegetative anthocyanins, whereas TT19-4 cDNA cannot complement the proanthocyanidin and pale seed coat phenotype of tt19-1. Both recombinant TT19 and TT19-4 enzymes are functional GSTs and are localized in the cytosol, but TT19 did not function with wide range of flavonoids and natural products to produce conjugation products. We suggest that the dark seed coat of Arabidopsis is related to soluble proanthocyanidin content and that quercetin holds the key to the function of TT19. In addition, TT19 appears to have a 5' GSH-binding domain influencing both anthocyanin and proanthocyanidin accumulation and a 3' domain affecting proanthocyanidin accumulation by a single amino acid substitution.     

基于机器学习的医学影像分析在药物研发和精准医疗方面的应用

MRI,PET,和CT等医学影像在新药研发和精准医疗中起着越来越重要的作用。影像技术可以被用来诊断疾病,评估药效,选择适应患者,或者确定用药剂量。 随着人工智能技术的发展,特别是机器学习以及深度学习技术在医学影像中的应用,使得我们可以用更短的时间,更少的放射剂量获取更高质量的影像。这些技术还可以帮助放射科医生缩短读片时间,提高诊断准确率。除此之外,机器学习技术还可以提高量化分析的可行性和精度,帮助建立影像与基因以及疾病的临床表现之间的关系。首先根据不同形态的医学影像,简单介绍他们在药物研发和精准医疗中的应用。并对机器学习在医学影像中的功能作一概括总结。最后讨论这个领域的挑战和机遇。     

蓝藻型富营养湖泊藻量的昼夜变化节律

杭州西湖为蓝藻型富营养湖泊,根据1980年9月及11月二次昼夜分层采样调查,该湖浮游藻在一昼夜中有二次上下垂直移位,使近表层藻量形成规则或不规则的双峰型昼夜变化曲线,双峰分别出现在日照开始与日落后2h左右,认为昼夜光暗交替与其昼夜变化有一定相关关系,同时,双峰的形成与蓝藻门优势藻种对光照强度的适应性能相关。文中对其优势藻种的浮沉与日照关系作了讨论。     

花色形成与花生长的调控

结合笔者的研究结果,对光、糖和GAs在花生长及花色形成中的作用和可能的调节机制进行了综述。光通过光受体介导的高辐照度反应(HIR)和光合作用调控花生长及花色素苷合成;糖作为碳源和渗透调节因子,影响花瓣细胞的生长及花色素苷积累,依赖己糖激酶的信号途径可能在糖的调控中起作用;GAs通过调节特异基因的转录间接地诱导花色素苷合成途径中结构基因的表达。     

辽西樟子松人工林净生态系统碳交换

樟子松是三北地区造林的主要树种之一,研究樟子松人工林净生态系统碳交换(NEE)及其影响要素对理解我国人工林碳平衡有重要意义。本研究以辽西樟子松人工林为对象,采用涡度相关系统及其配套设备于2020年对樟子松人工林NEE和环境要素进行了原位连续观测。结果表明: 在0.5 h尺度上,1—12月夜间为碳源,白天为碳汇,且受干旱影响5—8月下午碳吸收受到明显抑制。在日尺度上,受干旱影响,控制夜间NEE季节动态的主要要素为土壤温度和土壤湿度,控制白天NEE季节动态的主要要素为土壤湿度和饱和水汽压差;土壤干旱时降水可促进夜间和白天NEE,并导致光合呼吸参数升高。在月尺度上,白天NEE与表观量子利用效率和最大光合速率均呈显著负相关,当空气温度小于5 ℃时,10 ℃生态系统呼吸和生态系统呼吸温度敏感性随空气温度降低而呈线性增加。2020年辽西樟子松人工林NEE积累量为-145.17 g C·m^-2,表现为弱碳汇。     

附生植物石斛的株丛生长及营养繁殖特征

石斛(Dendrobium nobile Lindl.)为兰科多年生附生性草本植物,特化的假鳞茎是其营养贮藏器官,通过假鳞茎可实现克隆生长。该研究以野外调查发现的石斛株丛为研究材料,比较不同等级株丛假鳞茎合轴生长和高位腋芽的差异,分析高位株丛的定植方式,探讨石斛株丛生长及营养繁殖对附生环境的适应策略。结果显示:(1)石斛株丛的生长和扩大通过合轴生长的营养繁殖方式进行,假鳞茎基部具有2~3个储备芽,每年萌发1~2个新芽,随着生长年限的增加,形成大小不一的株丛。(2)株丛具有典型的高位腋芽营养繁殖特性,且主要形成于假鳞茎密集和老根密布的大株丛。(3)高位株丛母茎一端附着于附主树种上,在母茎软化和高位株丛的重力作用下,缩短了高位株丛与附主的距离,使其根系能够触及附主,完成高位株丛的定植。研究表明,附生植物石斛通过假鳞茎合轴生长的营养繁殖方式来增强并延续株丛寿命,高位腋芽的频发是株丛假鳞茎对拥挤等逆境的响应,高位株丛的定植依赖于母茎,这也是石斛对附生环境的一种生态适应策略。     

基质氮磷含量对菹草生长与繁殖的影响

通过设计6个营养水平的沉积物处理,研究了沉积物中氮磷含量对菹草萌发、生长和繁殖的影响.结果表明:沉积物氮磷含量对菹草石芽的萌发无影响,萌发率均达到100%;随着沉积物中氮磷含量的增加,植物组织氮含量增加,并趋于稳定,磷含量呈现缓慢上升趋势,而植株体内氮磷比值下降,同时,菹草叶片的初始荧光产量(Fo)降低,最大量子产率(Fv/Fm)不断增加,达到一定限度后略有下降,表明菹草光合能力随沉积物氮磷含量的增加而提高,而过高的氮磷水平会降低光合能力;快速光曲线显示,菹草能有效地利用弱光,强光下易出现光抑制现象,但高氮磷营养水平的沉积物可以提高菹草对强光的耐受能力.此外,高氮磷含量也能提高菹草总生物量,但降低了菹草的根茎比.菹草无性生殖能力随氮磷水平的提高不断增强,繁殖策略也得到优化,出现了有性生殖,但结实率平均仅为19.6%.     

Determination of the functional epitopes of human interleukin-18-binding protein by site-directed mutagenesis

The human interleukin (IL)-18-binding protein (hIL-18BP) is a naturally occurring antagonist of IL-18, a proinflammatory cytokine that is related to IL-1beta and has an important role in defense against microbial invaders. As its name implies, the hIL-18BP binds to IL-18 with high affinity and prevents the interaction of IL-18 with its receptor. We genetically modified the C terminus of hIL-18BP by appending a 15-amino acid biotinylation recognition site and a six-histidine tag and then performed site-directed mutagenesis to determine the functional epitopes that mediate efficient binding to IL-18. The mutated IL-18BPs were secreted from mammalian cells, captured by metal affinity chromatography, biotinylated in situ, eluted, and immobilized on streptavidin-coated chips. Using surface plasmon resonance, we identified seven amino acids of hIL-18BP which, when changed individually to alanine, caused an 8-750-fold decrease in binding affinity, largely because of increased off-rates. These seven amino acids localized to the predicted beta-strand c and d of hIL-18BP immunoglobulin-like domain, and most had hydrophobic side chains. Just two amino acids, tyrosine 97 and phenylalanine 104, contributed approximately 50% of the binding free energy. Information obtained from these studies could contribute to the design of molecular antagonists of IL-18 for treatment of inflammatory diseases.     

Epac‐2 ameliorates spontaneous colitis in Il‐10 −/− mice by protecting the intestinal barrier and suppressing NF‐κB/MAPK signalling

Intestinal barrier dysfunction and intestinal inflammation interact in the progression of Crohn''s disease (CD). A recent study indicated that Epac‐2 protected the intestinal barrier and had anti‐inflammatory effects. The present study examined the function of Epac‐2 in CD‐like colitis. Interleukin‐10 gene knockout (Il‐10 ^−/−) mice exhibit significant spontaneous enteritis and were used as the CD model. These mice were treated with Epac‐2 agonists (Me‐cAMP) or Epac‐2 antagonists (HJC‐0350) or were fed normally (control), and colitis and intestinal barrier structure and function were compared. A Caco‐2 and RAW 264.7 cell co‐culture system were used to analyse the effects of Epac‐2 on the cross‐talk between intestinal epithelial cells and inflammatory cells. Epac‐2 activation significantly ameliorated colitis in mice, which was indicated by reductions in the colitis inflammation score, the expression of inflammatory factors and intestinal permeability. Epac‐2 activation also decreased Caco‐2 cell permeability in an LPS‐induced cell co‐culture system. Epac‐2 activation significantly suppressed nuclear factor (NF)‐κB/mitogen‐activated protein kinase (MAPK) signalling in vivo and in vitro. Epac‐2 may be a therapeutic target for CD based on its anti‐inflammatory functions and protective effects on the intestinal barrier.