拟南芥 MeIAA 抗性突变体的筛选和初步图位克隆分析

生长素是最重要的植物激素之一, 参与了植物生长发育的各个方面。植物体内游离的IAA是生长素的主要活性形式, 在IAA甲基转移酶1(IAMT1)的作用下, IAA可以转变为IAA甲酯 (MeIAA)。MeIAA本身没有活性, 在植物体内的MeIAA酯解酶作用下可以重新转变为IAA。 MeIAA是非极性分子, 能够在植物体内自由扩散。利用MeIAA的这种特殊性质筛选突变体, 可以分离到MeIAA代谢途径或者IAA途径中新的成分。我们对拟南芥种子进行EMS诱变, 通过观察黑暗下下胚轴的生长情况, 筛选MeIAA的抗性突变体。我们成功分离到了8株可能的抗性突变体, 并对其中的一个Methyl -IAA resistant 1 (mir1) 突变体进行了深入分析。MeIAA抗性突变体的筛选将为进一步了解MeIAA的代谢、IAA稳态调控和响应机理提供新的材料。     

Simultaneous saccharification and fermentation of acid-pretreated corncobs with a recombinant Saccharomyces cerevisiae expressing beta-glucosidase

To reduce the cellobiose inhibition of exoglucanase and endogulcanase and enhance cellulose hydrolysis during simultaneous saccharification and fermentation (SSF), a beta-glucosidase encoding gene named BGL1 was cloned from Saccharomycopsis fibuligera and integrated into the chromosomal rDNA region of the Saccharomyces cerevisiae industrial strain NAN-27 producing NAN-227. Compared with the parental strain, which had no detectable activity, the beta-glucosidase specific activity in NAN-227 was 1.02 IU/mg of protein. When cellobiose was used as the sole carbon source in a shake-flask, NAN-227 consumed 6.2g/L of cellobiose and produced 3.3g/L of ethanol in 48 h. The yield was 0.532 g/g. The parent strain only consumed 1.92 g/L of cellobiose and no ethanol was detected. During the SSF of acid-pretreated corncobs NAN-227 produced 20 g/L of ethanol at 72 h, which was similar to the parent strain when 20IU of beta-glucosidase/g of substrate was added.     

Genomics,molecular imaging,bioinformatics, and bio-nano-info integration are synergistic components of translational medicine and personalized healthcare research

Supported by National Science Foundation (NSF), International Society of Intelligent Biological Medicine (ISIBM), International Journal of Computational Biology and Drug Design and International Journal of Functional Informatics and Personalized Medicine, IEEE 7th Bioinformatics and Bioengineering attracted more than 600 papers and 500 researchers and medical doctors. It was the only synergistic inter/multidisciplinary IEEE conference with 24 Keynote Lectures, 7 Tutorials, 5 Cutting-Edge Research Workshops and 32 Scientific Sessions including 11 Special Research Interest Sessions that were designed dynamically at Harvard in response to the current research trends and advances. The committee was very grateful for the IEEE Plenary Keynote Lectures given by: Dr. A. Keith Dunker (Indiana), Dr. Jun Liu (Harvard), Dr. Brian Athey (Michigan), Dr. Mark Borodovsky (Georgia Tech and President of ISIBM), Dr. Hamid Arabnia (Georgia and Vice-President of ISIBM), Dr. Ruzena Bajcsy (Berkeley and Member of United States National Academy of Engineering and Member of United States Institute of Medicine of the National Academies), Dr. Mary Yang (United States National Institutes of Health and Oak Ridge, DOE), Dr. Chih-Ming Ho (UCLA and Member of United States National Academy of Engineering and Academician of Academia Sinica), Dr. Andy Baxevanis (United States National Institutes of Health), Dr. Arif Ghafoor (Purdue), Dr. John Quackenbush (Harvard), Dr. Eric Jakobsson (UIUC), Dr. Vladimir Uversky (Indiana), Dr. Laura Elnitski (United States National Institutes of Health) and other world-class scientific leaders. The Harvard meeting was a large academic event 100% full-sponsored by IEEE financially and academically. After a rigorous peer-review process, the committee selected 27 high-quality research papers from 600 submissions. The committee is grateful for contributions from keynote speakers Dr. Russ Altman (IEEE BIBM conference keynote lecturer on combining simulation and machine learning to recognize function in 4D), Dr. Mary Qu Yang (IEEE BIBM workshop keynote lecturer on new initiatives of detecting microscopic disease using machine learning and molecular biology, http://ieeexplore.ieee.org/servlet/opac?punumber=4425386) and Dr. Jack Y. Yang (IEEE BIBM workshop keynote lecturer on data mining and knowledge discovery in translational medicine) from the first IEEE Computer Society BioInformatics and BioMedicine (IEEE BIBM) international conference and workshops, November 2-4, 2007, Silicon Valley, California, USA.     

Enhanced Electrocatalysis for Energy‐Efficient Hydrogen Production over CoP Catalyst with Nonelectroactive Zn as a Promoter

As a non‐toxic species, Zn fulfills a multitude of biological roles, but its promoting effect on electrocatalysis has been rarely explored. Herein, the theoretic predications and experimental investigations that nonelectroactive Zn behaves as an effective promoter for CoP‐catalyzed hydrogen evolution reaction (HER) in both acidic and alkaline media is reported. Density function theory calculations reveal that Zn doing leads to more thermal‐neutral hydrogen adsorption free energy and thus enhanced HER activity for CoP catalyst. Electrochemical tests show that a Zn_0.08Co_0.92P nanowall array on titanium mesh (Zn_0.08Co_0.92P/TM) needs overpotentials of only 39 and 67 mV to drive a geometrical catalytic current of 10 mA cm^‐2 in 0.5 m H₂SO₄ and 1.0 m KOH, respectively. This Zn_0.08Co_0.92P/TM is also superior in activity over CoP/TM for urea oxidation reaction (UOR), driving 115 mA cm^‐2 at 0.6 V in 1.0 m KOH with 0.5 m urea. The high HER and UOR activity of this bifunctional electrode enables a Zn_0.08Co_0.92P/TM‐based two‐electrode electrolyzer for energy‐saving hydrogen production, offering 10 mA cm^‐2 at a low voltage of 1.38 V with strong long‐term electrochemical stability.     

Synthesis of indazole based diarylurea derivatives and their antiproliferative activity against tumor cell lines

New series of indazole based diarylureas were synthesized and their anticancer activity against cancer cells H460, A549, OS-RC-2, HT-29, Lovo, HepG2, Bel-7402, SGC-7901 and MDA-MB-231 were examined. These derivatives of diarylureas, except azaindazole based diarylureas 5f, 5l and 5m, showed superior or similar activity against most of these selected cancer cell lines to the reference compound sorafenib. The effect of substituents on the indazole ring was also investigated. Derivatives with trifluoromenthy or halogen substituent on the indazole ring showed higher activity against the selected cancer cell lines than sorafenib. The acute toxicity assay showed that compounds 5a, 5b and 5i possessed lower toxicity than sorafenib. Compound 5i with 4-(trifluoromenthy)-1H-indazole and 4-(trifluoromenthy) benzene moieties exhibited the most potent anticancer activity.     

Distribution of endoglin in early human development reveals high levels on endocardial cushion tissue mesenchyme during valve formation

Endoglin is a component of the receptor complex for transforming growth factor (TGF)-β1 and TGF-β3. We analysed its expression by immunohistochemistry in human embryos at 4–8 weeks of gestation and in hearts ranging from 4–13 weeks old. We compared endoglin distribution with that of TGF-β receptors type I (TβR-I), type II (TβR-II) and betaglycan. Endoglin was found on endothelial cells in all tissues examined, consistent with its expression in adult blood vessels. TβR-I, TβR-II and betaglycan were observed on most cell types and had an overall similar pattern of distribution. Endoglin was detected on the endocardium as early as 4 weeks, but was absent from myocardium. It was present at high levels on the endocardial cushion tissue mesenchyme from 5–8 weeks’ gestation, during heart septation and valve formation, and subsequently decreased as the valves matured. Endoglin expression in heart extracts was confirmed by Western blot analysis. TβR-I, TβR-II and betaglycan were mostly found on cardiac myocytes, but were detectable at low levels on endocardium. They were expressed transiently on cushion mesenchyme, albeit at much lower levels than endoglin. All four components of the TGF-β receptor complex were detected by RT-PCR in embryonic heart. Thus transient up-regulation of the components of the TGF-β receptor complex, and particulartly of endoglin, is associated with heart septation and valve formation during early human development.     

Iodine Excess Induces Hepatic Steatosis Through Disturbance of Thyroid Hormone Metabolism Involving Oxidative Stress in BaLB/c Mice

Iodine excess is emerging as a new focus. A better understanding of its hazardous effects on the liver will be of great benefit to health. The aim of this study is to illustrate the effects of iodine excess on hepatic lipid homeostasis and explore its possible mechanisms. One hundred twenty BaLB/c mice were given iodine at different levels (0, 0.3, 0.6, 1.2, 2.4, and 4.8 mg I/L) in drinking water for 1 or 3 months. Lipid parameters and serum thyroid hormones were measured. Hepatic type 1 deiodinase activity and oxidative stress parameters were evaluated. The mRNA expression of sterol regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) was detected by real-time polymerase chain reaction. Dose-dependent increase of hepatic triglyceride content was detected (r?=?0.680, P?<?0.01) in iodine-loaded groups. Evident hepatic steatosis was observed in 2.4 and 4.8 mg I/L iodine-loaded groups. The activities of antioxidant enzymes (glutathione peroxidase and superoxide dismutase) were decreased, and the malondialdehyde level was increased by excessive iodine in both serum and liver in a dose-dependent manner, accompanying the decrease of hepatic D1 activity. That resulted in the increase of serum total thyroxine and the decrease of serum total triiodothyronine in iodine-loaded groups. The mRNA expression of SREBP-1c and FAS was increased in iodine-loaded groups in response to the change of serum triiodothyronine. Present findings demonstrated that iodine excess could dose dependently induce hepatic steatosis. Furthermore, our data suggested that the disturbance of thyroid hormone metabolism involving oxidative stress may play a critical role in iodine excess-induced hepatic steatosis.