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Functional Counterpart (functional + counterpart)
Selected AbstractsCorrelation of ,-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in ratsEXPERIMENTAL PHYSIOLOGY, Issue 3 2006Donatella Stilli We have analysed alterations of ,-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of ,-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of ,-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in ,-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance. [source] The archaeal Hjm helicase has recQ-like functions, and may be involved in repair of stalled replication forkGENES TO CELLS, Issue 2 2006Ryosuke Fujikane The archaeal Hjm is a structure-specific DNA helicase, which was originally identified in the hyperthermophilic archaeon, Pyrococcus furiosus, by in vitro screening for Holliday junction migration activity. Further biochemical analyses of the Hjm protein from P. furiosus showed that this protein preferably binds to fork-related Y-structured DNAs and unwinds their double-stranded regions in vitro, just like the E. coli RecQ protein. Furthermore, genetic analyses showed that Hjm produced in E. coli cells partially complemented the defect of functions of RecQ in a recQ mutant E. coli strain. These results suggest that Hjm may be a functional counterpart of RecQ in Archaea, in which it is necessary for the maintenance of genome integrity, although the amino acid sequences are not conserved. The functional interaction of Hjm with PCNA for its helicase activity further suggests that the Hjm works at stalled replication forks, as a member of the reconstituted replisomes to restart replication. [source] Identification of a protein, YneA, responsible for cell division suppression during the SOS response in Bacillus subtilisMOLECULAR MICROBIOLOGY, Issue 4 2003Yoshikazu Kawai Summary A knock-out mutant of the dinR gene that encodes the SOS regulon repressor in Bacillus subtilis was constructed. The yneA, yneB and ynzC genes transcribed divergently from the dinR gene were strongly induced in mutant cells. Northern hybridization analyses revealed that these genes collectively form an operon and belong to the SOS regulon. The simultaneous deletion of dinR and yneA suppressed the filamentous phenotype of the dinR mutant. Furthermore, although yneA is suppressed in the wild-type cell in the absence of SOS induction, artificial expression of the YneA protein using an IPTG-inducible promoter resulted in cell elongation. Disruption of yneA significantly reduced cell elongation after the induction of the SOS response by mitomycin C in dinR+ cells. These results indicate that the YneA protein is responsible for cell division suppression during the SOS response in B. subtilis. Localization of the FtsZ protein to the cell division site was reduced in dinR -disrupted or yneA -expressing cells, further suggesting that the YneA protein suppresses cell division through the suppression of FtsZ ring formation. Interestingly, the B. subtilis YneA protein is structurally and phylogenetically unrelated to its functional counterpart in Escherichia coli, SulA. [source] Significance of error-avoiding mechanisms for oxidative DNA damage in carcinogenesisCANCER SCIENCE, Issue 4 2007Teruhisa Tsuzuki Reactive oxygen species (ROS) are produced through normal cellular metabolism, and their formation is further enhanced by exposure to ionizing radiation and various chemicals. ROS attack DNA, and the resulting oxidative DNA damage is considered to contribute to aging, carcinogenesis and neurodegeneration. Among various types of oxidative DNA damage, 8-oxo-7,8-dihydroguanine (8-oxoguanine or 8-oxoG) is the most abundant, and plays significant roles in mutagenesis because of its ability to pair with adenine as well as cytosine. Enzymatic activities that may be responsible for preventing 8-oxoG-evoked mutations were identified in mammalian cells. We have focused on the following three enzymes: MTH1, OGG1 and MUTYH. MTH1 is a mammalian ortholog of Escherichia coli MutT, which hydrolyzes 8-oxo-dGTP to its monophosphate form in nucleotide pools, thereby preventing incorporation of the mutagenic substrate into DNA. OGG1, a functional counterpart of E. coli MutM, has an 8-oxoG DNA glycosylase activity. MUTYH, a mammalian ortholog of E. coli MutY, excises an adenine paired with 8-oxoG. These three enzymes are thought to prevent mutagenesis caused by 8-oxoG in mammals. To analyze the functions of mammalian MTH1 (Mth1), OGG1 (Ogg1) and MUTYH (Mutyh) in vivo, we established mutant mice for these three enzymes by targeted mutagenesis, and investigated spontaneous tumorigenesis as well as mutagenesis. Here we discuss our recent investigation of mutagenesis and carcinogenesis in these mutant mice. (Cancer Sci 2007; 98: 465,470) [source] Ribosomal DNA pseudogenes are widespread in the eucalypt group (Myrtaceae): implications for phylogenetic analysisCLADISTICS, Issue 2 2008Michael J. Bayly Pseudogenes from the 18S,5.8S,26S cistron of nuclear ribosomal DNA are reported in the eucalypt group (Myrtaceae), which includes seven genera. Putative pseudogenes are identified by a range of sequence comparisons including: the number of CpG and CpNpG methylation sites, GC content, estimated secondary structure stability of internal transcribed spacer transcripts, the presence of conserved motifs, patterns of sequence relationships and inferred substitution patterns. These comparisons indicate that pseudogenes are widespread, being evident in Eucalyptus (subgenera Eucalyptus and Eudesmia), Corymbia (extracodical sections Rufaria, Ochraria and Blakearia), Angophora, Stockwellia quadrifida and Arillastrum gummiferum. At least six sequences used in previous phylogenetic studies are identified as pseudogenes, and a further 10 pseudogenes are newly sequenced here. Gene trees place pseudogenes in a number of distinct lineages: pseudogenes from Eucalyptus group with other Eucalyptus sequences, those from Corymbia and Angophora group with other Corymbia/Angophora sequences, that from Stockwellia groups with other sequences from the Eucalyptopsis group, and that from Arillastrum is placed as sister to the other included sequence of Arillastrum. Some pseudogenes in Eucalyptus, Corymbia and Angophora represent "deep" ribosomal DNA paralogues that pre-date species differentiation in these groups, and a recombination analysis shows no evidence of recombination between putative pseudogenes and their functional counterparts. The presence of divergent paralogues presents both challenges and opportunities for the reconstruction of eucalypt phylogenies using ribosomal DNA sequences. Phylogenetic data sets should include only orthologous sequences, but different paralogues potentially provide additional, independent, character sets for phylogenetic analyses. © The Willi Hennig Society 2007. [source] | ||||||||||