大豆高光效育种研究进展

多年的研究证明,提高光合效率是提高大豆产量的重要途径.在高产条件下,高光效大豆(Glycine max L. Merr.)品种与一般品种相比可提高产量30%～40%,表明高光效育种有着广阔的发展前景.高光效育种虽然未能缩短育种时间,但为达到预定的高光效目标提供了"实时"监测,可免除目标的偏离,从而达到高光效与高产的同步提高.大豆叶片与豆荚均存在着高活性的有限的C4途径循环,因此,通过常规育种或基因工程技术提高C4途径酶的表达能力,可能是提高C3植物光合效率的新突破点.     

13C NMR在马利筋族植物C21甾类成分结构研究中的应用

本文介绍了＾１３ＣＮＭＲ在以列筋族植物Ｃ２１甾类成分甙元类型工基的确定、糖的种类、连接顺序的判断等方面的应用。     

Influence of microgravity on ultrastructure and storage reserves in seeds of Brassica rapa L.

Successful plant reproduction under spaceflight conditions has been problematic in the past. During a 122 d opportunity on the Mir space station, full life cycles of Brassica rapa L. were completed in microgravity in a series of three experiments in the Svet greenhouse. Ultrastructural and cytochemical analyses of storage reserves in mature dry seeds produced in these experiments were compared with those of seeds produced during a high-fidelity ground control. Additional analyses were performed on developing Brassica embryos, 15 d post pollination, which were produced during a separate experiment on the Shuttle (STS-87). Seeds produced on Mir had less than 20% of the cotyledon cell number found in seeds harvested from the ground control. Cytochemical localization of storage reserves in mature cotyledons showed that starch was retained in the spaceflight material, whereas protein and lipid were the primary storage reserves in ground control seeds. Protein bodies in mature cotyledons produced in space were 44% smaller than those in the ground control seeds. Fifteen days after pollination, cotyledon cells from mature embryos formed in space had large numbers of starch grains, and protein bodies were absent, while in developing ground control seeds at the same stage, protein bodies had already formed and fewer starch grains were evident. These data suggest that both the late stage of seed development and maturation are changed in Brassica by growth in a microgravity environment. While gravity is not absolutely required for any step in the plant life cycle, seed quality in Brassica is compromised by development in microgravity.     

应用三元递减法筛选特异性心脏生长相关基因

心脏是由胚胎干细胞特异性分化而来的 ,但其分化的分子生物学机制尚不十分了解 .为建立一种新的筛选特异性心脏相关基因的方法 ,克隆特异性心脏生长相关基因 .从胚胎心、成年心和去胎心的胚胎中提取 m RNA,建立胎心 /成年心和胎心 /胎身两个递减性 c DNA文库 ,通过 DNA芯片和微阵列杂交筛选和克隆 ,建立了三元递减克隆的新方法 .获得了一个全长为 1 0 0 6 bp可编码1 94个氨基酸的新的与心脏生长相关的基因 ,它是 LIM家族的新成员 ,可特异性在心肌细胞表达 ,并可促进心肌细胞的生长 .结果表明 ,三元递减筛选法可以应用于寻找新的组织特异性表达的基因 .并且获得了一个新的与心脏生长相关的新基因 ,它可能在心肌生长和心肌肥厚的发生中发挥重要作用     

Genomic convergence underlying high-altitude adaptation in alpine plants

Evolutionary convergence is one of the most striking examples of adaptation driven by natural selection.However, genomic evidence for convergent adaptation to extreme environments remains scarce.Here, we assembled reference genomes of two alpine plants, Saussurea obvallata(Asteraceae)and Rheum alexandrae(Polygonaceae), with 37,938 and 61,463 annotated protein-coding genes. By integrating an additional five alpine genomes,we elucidated genomic convergence underlying high-altitude adaptation in al...     

Advanced glycation end products induce senescence of atrial myocytes and increase susceptibility of atrial fibrillation in diabetic mice

Diabetes mellitus (DM) is a common chronic metabolic disease caused by significant accumulation of advanced glycation end products (AGEs). Atrial fibrillation (AF) is a common cardiovascular complication of DM. Here, we aim to clarify the role and mechanism of atrial myocyte senescence in the susceptibility of AF in diabetes. Rapid transesophageal atrial pacing was used to monitor the susceptibility of mice to AF. Whole‐cell patch‐clamp was employed to record the action potential (AP) and ion channels in single HL‐1 cell and mouse atrial myocytes. More importantly, anti‐RAGE antibody and RAGE‐siRNA AAV9 were used to investigate the relationship among diabetes, aging, and AF. The results showed that elevated levels of p16 and retinoblastoma (Rb) protein in the atrium were associated with increased susceptibility to AF in diabetic mice. Mechanistically, AGEs increased p16/Rb protein expression and the number of SA‐β‐gal‐positive cells, prolonged the action potential duration (APD), reduced protein levels of Cav1.2, Kv1.5, and current density of I _Ca,L , I _Kur in HL‐1 cells. Anti‐RAGE antibody or RAGE‐siRNA AAV9 reversed these effects in vitro and in vivo, respectively. Furthermore, downregulating p16 or Rb by siRNA prevented AGEs‐mediated reduction of Cav1.2 and Kv1.5 proteins expression. In conclusion, AGEs accelerated atrial electrical remodeling and cellular senescence, contributing to increased AF susceptibility by activating the p16/Rb pathway. Inhibition of RAGE or the p16/Rb pathway may be a potential therapeutic target for AF in diabetes.     

Synthesis and Antibacterial Activity Evaluation of Biphenyl and Dibenzofuran Derivatives as Potential Antimicrobial Agents against Antibiotic-Resistant Bacteria

The escalating prevalence of antibiotic-resistant bacteria has led to a serious global public health problem; therefore, there is an urgent need for the development of structurally innovative antibacterial agents. In our study, a series of biphenyl and dibenzofuran derivatives were designed and synthesized by Suzuki-coupling and demethylation reactions in moderate to excellent yields (51–94% yield). Eleven compounds exhibited potent antibacterial activities against the prevalent antibiotic-resistant Gram-positive and Gram-negative pathogens, among which compounds 4′-(trifluoromethyl)-[1,1′-biphenyl]-3,4,5-triol (6i) and 5-(9H-carbazol-2-yl) benzene-1,2,3-triol (6m) showed the most potent inhibitory activities against methicillin-resistant Staphylococcus aureus and multidrug-resistant Enterococcus faecalis with MIC (minimum inhibitory concentration) values as low as 3.13 and 6.25 μg/mL, respectively. Compounds 3′,5′-dimethyl-[1,1′-biphenyl]-3,4,4′,5-tetraol (6e), 4′-fluoro-[1,1′-biphenyl]-3,4,5-triol (6g), and 4′-(trifluoromethyl)-[1,1′-biphenyl]-3,4,5-triol (6i) showed comparable inhibitory activities with ciprofloxacin to Gram-negative bacterium carbapenems-resistant Acinetobacter baumannii. Study of the structure–activity relationship indicated that a strong electron-withdrawing group on the A ring and hydroxyl groups on the B ring of biphenyls were beneficial to their antibacterial activities, and for benzo-heterocycles, N-heterocycle exhibited optimal antibacterial activity. These results can provide novel structures of antibacterial drugs chemically different from currently known antibiotics and broaden prospects for the development of effective antibiotics against antibiotic-resistant bacteria.     

A novel methylated cation channel TRPM4 inhibited colorectal cancer metastasis through Ca2+/Calpain-mediated proteolysis of FAK and suppression of PI3K/Akt/mTOR signaling pathway

Colorectal cancer (CRC) is an aggressive malignancy with poor prognosis. It is imperative to elucidate the potential molecular mechanisms that regulate CRC cell aggressiveness. In present study, the transient receptor potential melastatin 4 (TRPM4), a calcium-activated nonselective cation channel, is downregulated in CRC as a novel methylated tumor suppressor gene (TSG). The reduced mRNA level of TRPM4 is due to the epigenetic methylation of its promoter CpG island (CGI). Moreover, ectopic expression of TRPM4 inhibited tumor growth and metastasis both in vitro and in vivo. Our experiments also demonstrate that TRPM4 restructures the CRC cytoskeleton and activates the Ca²⁺-mediated calpain pathway through enhancing calcium influx. The western blot analysis shows that the expression of focal adhesion kinase (FAK), a calpain-mediated proteolytic substrate, is markedly suppressed after ectopic overexpression of TRPM4, besides, Akt (also known as protein kinase B, PKB), phosphatidylinositol 3-kinase (PI3K) as well as its central target mTOR have significantly decreased expression accompanied by elevated E-cadherin and restrained matrix metalloproteinases (MMP2/MMP9) expression. The inhibition of protease calpain effectively relieves the retard of FAK/Akt signals and reverses the migration suppression of TRPM4. Taken together, TRPM4, identified as a novel methylated TSG, employs intracellular Ca²⁺ signals to activate calpain-mediated cleavage of FAK and impede CRC migration and invasion through modulating the PI3K/Akt/mTOR signaling cascade, providing the first evidence that TRPM4 is likely to be a significant biomarker and potential target for CRC therapy.