Cloning and sequence of UK bovine rotavirus gene segment 7: marked sequence homology with simian rotavirus gene segment 8.

The genome of the UK bovine rotavirus, which consists of eleven segments of dsRNA was polyadenylated and reverse-transcribed into cDNA. Complementary cDNA strands were annealed and the termini of the duplexes completed using DNA polymerase I. Full-length DNA copies of RNA segments 7, 8 and 9 were cloned into the Pst I site of pBR322 and a clone containing the entire gene 7 was identified and sequenced. Gene 7 is 1059 nucleotides in length and contains a single long open reading frame capable of coding for a protein of 317 amino-acids. The known gene product of segment 7 is a protein with an estimated molecular weight of 33,000 daltons. When the UK bovine rotavirus gene 7 sequence was compared with the published data for the homologous gene (segment 8) of the simian rotavirus SA11, it was found to be identical to it in size and the arrangement of the proposed coding and non-coding regions, and very similar in nucleotide sequence (88% homology). Most of the base changes are silent and the predicted amino-acid sequences are almost identical (96% homology).     

Molecular basis of human hypertension: role of angiotensinogen.

Essential hypertension is a common human disease believed to result from the interplay of multiple genetic and environmental determinants. In genetic studies of two large panels of hypertensive sibships from widely separated geographical areas, we obtained evidence of genetic linkage between the angiotensinogen gene (AGT) and hypertension, demonstrated association of AGT molecular variants with the disease, and found significant differences in plasma concentrations of angiotensinogen among hypertensive subjects with different AGT genotypes. The corroboration and replication afforded by these results support the interpretation that molecular variants of AGT constitute inherited predispositions to essential hypertension in humans.     

农杆菌-植物间基因转移的分子基础

植物病原细菌多以Ⅲ型分泌系统运送毒性因子或无毒基因产物到植物细胞,但根癌农杆菌利用Ⅳ型分泌系统转移致瘤基因片断T-DNA到植物细胞核,并整合到植物基因组,使植物产生肿瘤,作者将介绍vir基因的诱导、T-DNA的加工、T-DNA的转移,以及T-复合体运输的装备等方面的最新研究进展,以探讨农杆菌-植物间基因转移的分子基础,研究该系统转移基因的分子基础将有利于开发和改良植物遗传工程的载体工具;另外,农杆菌-植物作为一种模式植物病害系统,其研究也为植物-病原菌的基础理论研究提供参考。由于有些人体病原细菌也采用Ⅳ型分泌系统运送毒性因子到人体细胞,研究农杆菌-植物间的基因转移系统也有利于医学研究。     

Genetic basis of virulence in Shigella species.

Shigella species and enteroinvasive strains of Escherichia coli cause disease by invasion of the colonic epithelium, and this invasive phenotype is mediated by genes carried on 180- to 240-kb plasmids. In addition, at least eight loci on the Shigella chromosome are necessary for full expression of virulence. The products of these genes can be classified as (i) virulence determinants that directly affect the ability of shigellae to survive in the intestinal tissues, e.g., the aerobactin siderophore (iucABCD and iutA), superoxide dismutase (sodB), and somatic antigen expression (rfa and rfb); (ii) cytotoxins that contribute to the severity of disease, e.g., the Shiga toxin (stx) and a putative analog of this toxin (flu); and (iii) regulatory loci that affect the expression of plasmid genes, e.g., ompR-envZ, which mediates response to changes in osmolarity, virR (osmZ), which mediates response to changes in temperature, and kcpA, which affects the translation of the plasmid virG (icsA) gene which is associated with intracellular bacterial mobility and intracellular bacterial spread. A single plasmid regulatory gene (virF) controls a virulence-associated plasmid regulon including virG (icsA) and two invasion-related loci, i.e., (i) ipaABCD, encoding invasion plasmid antigens that may be structural components of the Shigella invasion determinant; and (ii) invAKJH (mxi), which is necessary for insertion of invasion plasmid antigens into the outer membrane.     

Molecular basis of human CD36 gene mutations

CD36 is a transmembrane glycoprotein of the class B scavenger receptor family. The CD36 gene is located on chromosome 7 q11.2 and is encoded by 15 exons. Defective CD36 is a likely candidate gene for impaired fatty acid metabolism, glucose intolerance, atherosclerosis, arterial hypertension, diabetes, cardiomyopathy, Alzheimer disease, and modification of the clinical course of malaria. Contradictory data concerning the effects of antiatherosclerotic drugs on CD36 expression indicate that further investigation of the role of CD36 in the development of atherosclerosis may be important for the prevention and treatment of this disease. This review summarizes current knowledge of CD36 gene structure, splicing, and mutations and the molecular, metabolic, and clinical consequences of these phenomena.     

Molecular basis of bacterial virulence and survival within infected hosts and the environment

The EMBO–FEBS lecture course on the ‘Molecular Basis of Bacterial Virulence and Survival Within Infected Hosts and in the Environment’, organized by Pascale Cossart, Efstathios Gonos and Roberto Kolter, was held on the island of Spetsai, Greece, September 3–13, 2002.     

Genetic basis of influenza virus virulence: gene composition and virulence of reassortants between mouse-adapted and nonadapted strains from different subtypes

Reassortment analysis of the pneumovirulence for mice marker of influenza virus has been performed. The original A/USSR/90/77 (H1H1) influenza virus strain or its mouse-adapted variant were crossed with a variant of A/Aichi/2/68 (H3N2) influenza virus highly virulent for mice. The reassortant having HA gene of the original A/USSR/90/77 virus and the other genes of the highly virulent A/Aichi/2/68 strain was avirulent for mice, whereas a similar reassortant possessing HA gene of the mouse-adapted A/USSR/90/77 strain was as virulent as A/Aichi/2/68 parent virus. The reasortant having HA and M genes of A/Aichi/2/68 and other genes of the mouse-adapted A/USSR/90/77 was moderately virulent, resembling in this respect the latter parent. The data indicates that changes in the different genes in course of viral adaptation to mice result in a differential acquisition of virulence for mice.     

Roots: Molecular basis of gene expression: Origins from the Pajama experiment

The Pajama (Pardee, Jacob, Monod) experiment provided a breakthrough in our understanding of the molecular mechanisms by which gene expression is regulated. Today, twenty-five years later it provides a paradigm for thinking about problems of gene expression, such as growth regulation and differentiation. From this experiment emerged entities such as repressors, regulatory genes, the operon as a group of jointly controlled genes, and messenger RNA.