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Selected AbstractsBiomarkers for exposure to estrogenic compounds: Gene expression analysis in zebrafish (Danio rerio)ENVIRONMENTAL TOXICOLOGY, Issue 1 2008Ulf Kausch Abstract Gene expression analyses in male zebrafish (Danio rerio) were carried out using microarray technique and quantitative polymerase chain reaction. Genes responding to the exposure to 17,-estradiol, bisphenol A and genistein were identified, among them genes involved in metabolism, reproductional and developmental processes. Threshold levels of 17,-estradiol (200 ng/L), bisphenol A (2000 ,g/L), and genistein (5000 ,g/L) for the upregulation of the vtg1 gene in short-time exposures (11 days) were determined by qPCR. 14k microarrays were used to generate complete lists of genes regulated by these estrogenic compounds. For this purpose, liver samples from 10 exposed zebrafish and 10 controls were processed. In this case the expressions of 211 genes were significantly regulated by 17,-estradiol, 47 by bisphenol A and 231 by genistein. Furthermore, it is shown that fish exposed to 17,-estradiol and genistein have similarities in their gene expression patterns, whereas bisphenol A apparently affected gene expression in a different way. Only genes coding for egg-yolk precursor protein vitellogenin were found to be regulated by all three compounds, which shows that these genes are the only suitable markers for exposure to different estrogenic compounds. The regulated genes were assigned to gene ontology classes. All three estrogenic compounds regulated genes mainly involved in primary and cellular metabolism, but genistein regulated several genes involved in cell cycle-regulation and bisphenol A several genes involved in protein biosynthesis. Genistein also upregulated the expression of four eggshell proteins, which can be used as biomarkers for exposure to this chemical. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2008. [source] A green light-absorbing phycoerythrin is present in the high-light-adapted marine cyanobacterium Prochlorococcus sp.ENVIRONMENTAL MICROBIOLOGY, Issue 10 2005Summary In the high-light-adapted unicellular marine cyanobacterium Prochlorococcus sp. MED4 the cpeB gene is the only gene coding for a structural phycobiliprotein. The absence of any other phycoerythrin gene in the fully sequenced genome of this organism, the previous inability to detect a gene product, and the mutation of two out of four cysteine residues, normally involved in binding chromophores, suggested that MED4- cpeB might not code for a functional protein. Here, transcription of MED4- cpeB at a low level was detected and the transcriptional start site was mapped. Enrichment of the protein identified phycoerythrobilin as its sole chromophore in vivo, which was confirmed by chromophorylation assays in vitro using the recombinant protein. Phycourobilin is the major chromophore in low-light-adapted Prochlorococcus ecotypes such as strain SS120. Therefore, spectrally tuned phycoerythrins are a characteristic feature of distinct Prochlorococcus ecotypes. Further in vitro mutagenesis experiments replacing one or both cysteines C61R/C82S by arginine or serine, respectively, revealed that only Cys82 is required for chromophore binding. Thus, an unusual green light-absorbing phycoerythrin evolved in the high-light-adapted ecotypes of Prochlorococcus, which potentially serves as a photoreceptor. [source] The mouse MPTP model: gene expression changes in dopaminergic neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2003Kati Kühn Abstract Parkinson's disease (PD) is a common neurodegenerative disorder, characterized by the progressive loss of dopaminergic neurons in the substantia nigra. Although valuable animal models have been developed, our knowledge of the aetiology and pathogenic factors implicated in PD is still insufficient to develop causal therapeutic strategies aimed at halting its progression. The neurotoxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is one of the most valuable models for analysing pathological aspects of PD. In this paper we studied the gene expression patterns underlying the pathogenesis of MPTP-induced neurodegeneration. We treated young and old C57BL/6 mice with different schedules of MPTP to induce degenerative processes that vary in intensity and time-course. During the first week after intoxication we used nonradioactive in situ -hybridization to investigate the expression patterns of genes associated with (i) dopamine metabolism and signalling; (ii) familial forms of PD; (iii) protein folding and (iv) energy metabolism. MPTP injections induced different severities of neuronal injury depending on the age of the animals and the schedule of administration as well as a significant degeneration in the striatum. In situ hybridization showed that MPTP intoxication initiated a number of gene expression changes that (i) were restricted to the neurons of the substantia nigra pars compacta; (ii) were correlated in intensity and number of changes with the age of the animals and the severity of histopathological disturbances; (iii) displayed in each a significant down-regulation by the end of one week after the last MPTP injection, but (iv) varied within one MPTP regimen in expression levels during the observation period. The subacute injection of MPTP into one-year-old mice induced the most severe changes in gene expression. All genes investigated were affected. However, ,-synuclein was the only gene that was exclusively up-regulated in MPTP-treated animals displaying cell death. [source] Potential pleiotropic effects of Mpdz on vulnerability to seizuresGENES, BRAIN AND BEHAVIOR, Issue 1 2004C. Fehr We previously mapped quantitative trait loci (QTL) responsible for approximately 26% of the genetic variance in acute alcohol and barbiturate (i.e., pentobarbital) withdrawal convulsion liability to a <,1 cM (1.8 Mb) interval of mouse chromosome 4. To date, Mpdz, which encodes the multiple PSD95/DLG/ZO-1 (PDZ) domain protein (MPDZ), is the only gene within the interval shown to have allelic variants that differ in coding sequence and/or expression, making it a strong candidate gene for the QTL. Previous work indicates that Mpdz haplotypes in standard mouse strains encode distinct protein variants (MPDZ1-3), and that MPDZ status is genetically correlated with severity of withdrawal from alcohol and pentobarbital. Here, we report that MPDZ status cosegregates with withdrawal convulsion severity in lines of mice selectively bred for phenotypic differences in severity of acute withdrawal from alcohol [i.e., High Alcohol Withdrawal (HAW) and Low Alcohol Withdrawal (LAW) lines] or pentobarbital [High Pentobarbital Withdrawal (HPW) and Low Pentobarbital Withdrawal (LPW) lines]. These analyses confirm that MPDZ status is associated with severity of alcohol and pentobarbital withdrawal convulsions. Using a panel of standard inbred strains of mice, we assessed the association between MPDZ status with seizures induced by nine chemiconvulsants. Our results show that MPDZ status is genetically correlated with seizure sensitivity to pentylenetetrazol, kainate and other chemiconvulsants. Our results provide evidence that Mpdz may have pleiotropic effects on multiple seizure phenotypes, including seizures associated with withdrawal from two classes of central nervous system (CNS) depressants and sensitivity to specific chemiconvulsants that affect glutaminergic and GABAergic neurotransmission. [source] Grey plumage colouration in the duck is genetically determined by the alleles on two different, interacting lociANIMAL GENETICS, Issue 1 2010Y. Gong Summary Based on the observation of a grey phenotype in the F1 generation from a cross between two white plumage duck varieties, the white Kaiya and the white Liancheng, we hypothesized a possible interaction between two autosomal loci that determine grey plumage. Using the parental and F1 individuals, seven testing combinations including five different F1 intercrosses (F2) and two different backcrosses (BC1 and BC2) were designed to test our hypothesis. It was demonstrated by chi-squared analysis that six test matings produced offspring in the expected ratios between the grey and white, with P- values ranging from 0.50 to 0.99. Another mating, where all white offspring were expected, produced 33 white individuals. These results verified that the interaction between two loci produced the grey phenotype. The C locus, which carries the recessive allele (c), was previously thought to be the only gene responsible for white plumage in the duck. This is the first report that an allele (t), carried by the white Liancheng at a different autosomal locus, also determines white plumage in ducks. Furthermore, the dominant alleles at both loci can interact with each other to produce the grey phenotype, and a new dark phenotype, observed in some F2 individuals, can be attributed to the dosage effect of the T allele. [source] Analysis of the VCX3A, VCX2 and VCX3B genes shows that VCX3A gene deletion is not sufficient to result in mental retardation in X-linked ichthyosisBRITISH JOURNAL OF DERMATOLOGY, Issue 3 2008S.A. Cuevas-Covarrubias Summary Background, X-linked ichthyosis (XLI), an inborn error of metabolism, is due to steroid sulphatase (STS) deficiency. Most patients with XLI harbour complete deletion of the STS gene and flanking sequences. The presence of low copy number repeats on either side of the STS gene seems to have a major role in the high frequency of these deletions. Some patients with XLI with terminal deletions of Xp22.3 involving marker DXS1139 and the STS gene show mental retardation (MR); VCX3A is the only gene located on this critical region. Objectives, To analyse the VCX3A, VCX, VCX2 and VCX3B genes in 80 unrelated Mexican patients with XLI with normal intelligence. Methods, STS activity was measured in the leucocytes using 7-[3H]-dehydroepiandrosterone sulphate as a substrate. Amplification of the regions from telomeric DXS89 to centromeric DXS1134 including both extremes of the STS and the VCX3A, VCX, VCX2 and VCX3B genes was performed using polymerase chain reaction. Results, No STS activity was detected in the patients with XLI (0·00 pmol mg,1 protein h,1). We observed two different deletion patterns: the first group included 62 patients with deletion of VCX3A and VCX genes. The second group included 18 patients with breakpoints at several regions on either side of the STS gene not including the VCX3A gene. Conclusions, These data indicate that more complex mechanisms, apart from possible VCX3A gene participation, are occurring in the genesis of MR in XLI, at least in the sample of Mexican patients analysed. [source] | ||||||||||