野生樱桃李扦插繁殖研究初报

以野生樱桃李的新梢为试材,采用不同的扦插基质、不同浓度的吲哚丁酸(IBA)、萘乙酸(NAA)和生根粉(ABR)对野生樱桃李插条进行扦插生根试验.试验结果表明,野生樱桃李在蛭石与河沙中的生根效果好于锯末中的生根,蛭石与河沙中插条的生根率接近,生根率分别达到了40.0%、39.6%,因此都可作为野生樱桃李扦插的适宜基质.适宜浓度NAA、IBA可以促进野生樱桃李的生根,浓度过低,达不到促进效果,浓度过高,则可能抑制了插条的生根,相比而言,效果NAA较好,其适宜处理浓度为200 mg/L.但各种激素处理后,无论生根率高低,对根的生长具有促进作用.     

用于筛选直链淀粉含量为中等的籼稻品种的分子标记

用PCR AccⅠ分子标记检测方法 ,检测了来自不同地区的 6 3个栽培水稻品种 (系 )蜡质基因第 1内含子剪接供体 1位碱基是G或是T。另外 ,还测定了这些水稻成熟种子的直链淀粉含量。结果显示该位置是G碱基的水稻品系成熟种子中直链淀粉含量均高于 2 0 % ,该位置是T的均低于 18%。在杂交育种过程中 ,这一分子标记可用于预测水稻植株种子的直链淀粉含量。对高直链淀粉含量的水稻亲本与中等直链淀粉含量的水稻亲本之间 5个籼型杂交组合F2 群体的分析表明 ,蜡质基因第 1内含子 1位碱基是G或是T与水稻种子中直链淀粉含量的高或低是紧密连锁 ,共同分离的。这些结果表明PCR AccⅠ分子标记检测方法可用于选育中等直链淀粉含量的籼稻新品系     

Two novel aminooligosaccharides isolated from the culture of Streptomyces coelicoflavus ZG0656 as potent inhibitors of alpha-amylase

Two novel aminooligosaccharides were separated from the culture filtrate of Streptomyces coelicoflavus ZG0656. Their chemical structures were determined by electrospray ionization tandem mass spectrometry (ESI-MS/MS) and 2D nuclear magnetic resonance (NMR) spectroscopy. Because of their acarviosine core structures, the names acarviostatins II23 and II13 were given to the novel compounds. The two acarviostatins were both mixed noncompetitive inhibitors of porcine pancreatic alpha-amylase (PPA), with inhibition constants (K(i)) of 0.009 microM (acarviostatin II23) and 0.010 microM (acarviostatin II13). Therefore, acarviostatin II23 and acarviostatin II13 are, respectively, 231 and 208 times more potent than acarbose.     

Checkpoint signaling, base excision repair, and PARP promote survival of colon cancer cells treated with 5-fluorodeoxyuridine but not 5-fluorouracil

The fluoropyrimidines 5-fluorouracil (5-FU) and FdUrd (5-fluorodeoxyuridine; floxuridine) are the backbone of chemotherapy regimens for colon cancer and other tumors. Despite their widespread use, it remains unclear how these agents kill tumor cells. Here, we have analyzed the checkpoint and DNA repair pathways that affect colon tumor responses to 5-FU and FdUrd. These studies demonstrate that both FdUrd and 5-FU activate the ATR and ATM checkpoint signaling pathways, indicating that they cause genotoxic damage. Notably, however, depletion of ATM or ATR does not sensitize colon cancer cells to 5-FU, whereas these checkpoint pathways promote the survival of cells treated with FdUrd, suggesting that FdUrd exerts cytotoxicity by disrupting DNA replication and/or inducing DNA damage, whereas 5-FU does not. We also found that disabling the base excision (BER) repair pathway by depleting XRCC1 or APE1 sensitized colon cancer cells to FdUrd but not 5-FU. Consistent with a role for the BER pathway, we show that small molecule poly(ADP-ribose) polymerase 1/2 (PARP) inhibitors, AZD2281 and ABT-888, remarkably sensitized both mismatch repair (MMR)-proficient and -deficient colon cancer cell lines to FdUrd but not to 5-FU. Taken together, these studies demonstrate that the roles of genotoxin-induced checkpoint signaling and DNA repair differ significantly for these agents and also suggest a novel approach to colon cancer therapy in which FdUrd is combined with a small molecule PARP inhibitor.     

Draft genome sequence of Streptomyces coelicoflavus ZG0656 reveals the putative biosynthetic gene cluster of acarviostatin family α-amylase inhibitors

Aims: The aims of this study are to obtain the draft genome sequence of Streptomyces coelicoflavus ZG0656, which produces novel acarviostatin family α‐amylase inhibitors, and then to reveal the putative acarviostatin‐related gene cluster and the biosynthetic pathway. Methods and Results: The draft genome sequence of S. coelicoflavus ZG0656 was generated using a shotgun approach employing a combination of 454 and Solexa sequencing technologies. Genome analysis revealed a putative gene cluster for acarviostatin biosynthesis, termed sct‐cluster. The cluster contains 13 acarviostatin synthetic genes, six transporter genes, four starch degrading or transglycosylation enzyme genes and two regulator genes. On the basis of bioinformatic analysis, we proposed a putative biosynthetic pathway of acarviostatins. The intracellular steps produce a structural core, acarviostatin I00‐7‐P, and the extracellular assemblies lead to diverse acarviostatin end products. Conclusions: The draft genome sequence of S. coelicoflavus ZG0656 revealed the putative biosynthetic gene cluster of acarviostatins and a putative pathway of acarviostatin production. Significance and Impact of the Study: To our knowledge, S. coelicoflavus ZG0656 is the first strain in this species for which a genome sequence has been reported. The analysis of sct‐cluster provided important insights into the biosynthesis of acarviostatins. This work will be a platform for producing novel variants and yield improvement.     

观赏羽衣甘蓝SSR标记分型与亲缘关系研究

观赏羽衣甘蓝凭借优良的观赏特性和抗逆性已经成为重要的冷季观赏植物。国内观赏羽衣甘蓝育种起步较晚,并且缺乏对种质资源遗传背景的系统研究。本研究应用SSR标记对不同类型的观赏羽衣甘蓝材料进行标记分型和亲缘关系分析。从99对均匀分布于甘蓝基因组的SSR引物中筛选出46对多态性好的引物,对27份不同类型的观赏羽衣甘蓝材料进行标记分型,共扩增出210个多态性位点,平均PIC值为0.58。进一步利用标记分型结果进行STRUCTURE群体结构、UPGMA聚类和聚类热图分析,结果显示3种分析结果基本一致,可以将27份材料分为圆叶、羽叶和皱叶3种类型,其中圆叶和羽叶类型的亲缘关系更近,与皱叶类型的亲缘关系较远;STRUCTURE分析还可以将双亲为不同类型的杂交种材料进行区分;聚类热图分析可以将标记分型结果形象的展示出来。本研究为进一步建立观赏羽衣甘蓝分子指纹图谱,明确种质资源的遗传背景,建立观赏羽衣甘蓝分子标记辅助选择育种体系,培育具有自主知识产权的新品种奠定基础。     

Loss to Clinic and Five-Year Mortality among HIV-Infected Antiretroviral Therapy Initiators

Missing outcome data due to loss to follow-up occurs frequently in clinical cohort studies of HIV-infected patients. Censoring patients when they become lost can produce inaccurate results if the risk of the outcome among the censored patients differs from the risk of the outcome among patients remaining under observation. We examine whether patients who are considered lost to follow up are at increased risk of mortality compared to those who remain under observation. Patients from the US Centers for AIDS Research Network of Integrated Clinical Systems (CNICS) who newly initiated combination antiretroviral therapy between January 1, 1998 and December 31, 2009 and survived for at least one year were included in the study. Mortality information was available for all participants regardless of continued observation in the CNICS. We compare mortality between patients retained in the cohort and those lost-to-clinic, as commonly defined by a 12-month gap in care. Patients who were considered lost-to-clinic had modestly elevated mortality compared to patients who remained under observation after 5 years (risk ratio (RR): 1.2; 95% CI: 0.9, 1.5). Results were similar after redefining loss-to-clinic as 6 months (RR: 1.0; 95% CI: 0.8, 1.3) or 18 months (RR: 1.2; 95% CI: 0.8, 1.6) without a documented clinic visit. The small increase in mortality associated with becoming lost to clinic suggests that these patients were not lost to care, rather they likely transitioned to care at a facility outside the study. The modestly higher mortality among patients who were lost-to-clinic implies that when we necessarily censor these patients in studies of time-varying exposures, we are likely to incur at most a modest selection bias.