58 research outputs found
Effect of cadmium on cytosine hydroxymethylation in gastropod hepatopancreas
5-Hydroxymethylcytosine (5hmC) is an important, yet poorly understood epigenetic DNA modification, especially in invertebrates. Aberrant genome-wide 5hmC levels have been associated with cadmium (Cd) exposure in humans, but such information is lacking for invertebrate bioindicators. Here, we aimed to determine whether this epigenetic mark is present in DNA of the hepatopancreas of the land snail Cantareus aspersus and is responsive to Cd exposure. Adult snails were reared under laboratory conditions and exposed to graded amounts of dietary cadmium for 14 days. Weight gain was used as a sublethal endpoint, whereas survival as a lethal endpoint. Our results are the first to provide evidence for the presence of 5hmC in DNA of terrestrial mollusks; 5hmC levels are generally low with the measured values falling below 0.03%. This is also the first study to investigate the interplay of Cd with DNA hydroxymethylation levels in a non-human animal study system. Cadmium retention in the hepatopancreas of C. aspersus increased from a dietary Cd dose of 1 milligram per kilogram dry weight (mg/kg d. wt). For the same treatment, we identified the only significant elevation in percentage of samples with detectable 5hmC levels despite the lack of significant mortalities and changes in weight gain among treatment groups. These findings indicate that 5hmC is an epigenetic mark that may be responsive to Cd exposure, thereby opening a new aspect to invertebrate environmental epigenetics
Breast cancer proteomics reveals correlation between estrogen receptor status and differential phosphorylation of PGRMC1
The neuromuscular system of Pycnophyes kielensis (Kinorhyncha: Allomalorhagida) investigated by confocal laser scanning microscopy
A guide to the Choquard equation
We survey old and recent results dealing with the existence and properties of
solutions to the Choquard type equations and some of its variants and extensions.Comment: 39 page
Population genomics of marine zooplankton
Author Posting. © The Author(s), 2017. This is the author's version of the work. It is posted here for personal use, not for redistribution. The definitive version was published in Bucklin, Ann et al. "Population Genomics of Marine Zooplankton." Population Genomics: Marine Organisms. Ed. Om P. Rajora and Marjorie Oleksiak. Springer, 2018. doi:10.1007/13836_2017_9.The exceptionally large population size and cosmopolitan biogeographic distribution that
distinguish many – but not all – marine zooplankton species generate similarly exceptional patterns of
population genetic and genomic diversity and structure. The phylogenetic diversity of zooplankton has
slowed the application of population genomic approaches, due to lack of genomic resources for closelyrelated
species and diversity of genomic architecture, including highly-replicated genomes of many
crustaceans. Use of numerous genomic markers, especially single nucleotide polymorphisms (SNPs), is
transforming our ability to analyze population genetics and connectivity of marine zooplankton, and
providing new understanding and different answers than earlier analyses, which typically used
mitochondrial DNA and microsatellite markers. Population genomic approaches have confirmed that,
despite high dispersal potential, many zooplankton species exhibit genetic structuring among geographic
populations, especially at large ocean-basin scales, and have revealed patterns and pathways of population
connectivity that do not always track ocean circulation. Genomic and transcriptomic resources are
critically needed to allow further examination of micro-evolution and local adaptation, including
identification of genes that show evidence of selection. These new tools will also enable further
examination of the significance of small-scale genetic heterogeneity of marine zooplankton, to
discriminate genetic “noise” in large and patchy populations from local adaptation to environmental
conditions and change.Support was provided by the
US National Science Foundation to AB and RJO (PLR-1044982) and to RJO (MCB-1613856); support to
IS and MC was provided by Nord University (Norway)
Deep developmental transcriptome sequencing uncovers numerous new genes and enhances gene annotation in the sponge Amphimedon queenslandica
Applications of In Vivo Imaging in the Evaluation of the Pathophysiology of Viral and Bacterial Infections and in Development of Countermeasures to BSL3/4 Pathogens
Mutations in the proenteropeptidase gene are the molecular cause of congenital enteropeptidase deficiency
Enteropeptidase (enterokinase [E.C.3.4.21.9]) is a serine protease of the intestinal brush border in the proximal small intestine. It activates the pancreatic proenzyme trypsinogen, which, in turn, releases active digestive enzymes from their inactive pancreatic precursors. Congenital enteropeptidase deficiency is a rare recessively inherited disorder leading, in affected infants, to severe failure to thrive. The genomic structure of the proenteropeptidase gene (25 exons, total gene size 88 kb) was characterized in order to perform DNA sequencing in three clinically and biochemically proved patients with congenital enteropeptidase deficiency who were from two families. We found compound heterozygosity for nonsense mutations (S712X/R857X) in two affected siblings and found compound heterozygosity for a nonsense mutation (Q261X) and a frameshift mutation (FsQ902) in the third patient. In accordance with the biochemical findings, all four defective alleles identified are predicted null alleles leading to a gene product not containing the active site of the enzyme. These data provide first evidence that proenteropeptidase-gene mutations are the primary cause of congenital enteropeptidase deficiency
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