The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation.

The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation. Abstract Text:

Dee R Denver,Seth Feinberg,Catherine Steding,Matthew Durbin,Michael Lynch,

Mutation is a central biological process whose rates and spectra are influenced by a variety of complex and interacting forces. Although DNA repair pathways are generally known to play key roles in maintaining genetic stability, much remains to be understood about the relative roles of different pathways in preventing the accumulation of mutations and the extent of heterogeneity in pathway-specific repair efficiencies across different genomic regions. In this study we examine mutation processes in base excision repair-deficient (nth-1) and nucleotide excision repair-deficient (xpa-1) Caenorhabditis elegans mutation-accumulation (MA) lines across 24 regions of the genome and compare our observations to previous data from mismatch repair-deficient (msh-2 and msh-6) and wild-type (N2) MA lines. Drastic variation in both average and locus-specific mutation rates, ranging two orders of magnitude for the latter, was detected among the four sets of repair-deficient MA lines. Our work provides critical insights into the relative roles of three DNA repair pathways in preventing C. elegans mutation accumulation and provides evidence for the presence of pathway-specific DNA repair territories in the C. elegans genome.

The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation. Publishing Authors By Initials

DR Denver,S Feinberg,C Steding,M Durbin,M Lynch,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Genetics

VOLUME: 174

Page Numbers: 57-65

Journal Abbreviation:

ISSN: 0016-6731

DAY: 18

MONTH: 06

YEAR: 2006

The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 374636

The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation.

AFFILIATION: Department of Biology, Indiana University, Bloomington, Indiana 47405, USA. denver@cgrb.oregonstate.edu

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Genetics

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation Related Publications

• Amphibian lipid levels at metamorphosis correlate to post-metamorphic terrestrial survival.
• Brain-derived neurotrophic factor promotes long-term potentiation-related cytoskeletal changes in adult hippocampus.
• Changes in synaptic morphology accompany actin signaling during LTP.
• Chronic hypersensitivity pneumonitis: CT features comparison with pathologic evidence of fibrosis and survival.
• Clinical selection of candidates for mutational testing for cancer susceptibility.
• Current and emerging strategies for the management of sarcoidosis.
• Dietary fish oil deactivates a growth-promoting signaling pathway in hepatoma 7288CTC in Buffalo rats.
• Diindolylquinoxalines: effective indole-based receptors for phosphate anion.
• ENG mutations in MADH4/BMPR1A mutation negative patients with juvenile polyposis.
• Evidence that long-term potentiation occurs within individual hippocampal synapses during learning.
• Familial genes in sporadic disease: common variants of alpha-synuclein gene associate with Parkinson's disease.
• Follicular development during early pregnancy and the estrous cycle of the sow.
• Fyn-mediated phosphorylation of NR2B Tyr-1336 controls calpain-mediated NR2B cleavage in neurons and heterologous systems.
• GAD antibody positive paraneoplastic stiff person syndrome in a patient with renal cell carcinoma.
• Global analysis of alternative splicing during T-cell activation.
• Grade III Gliomas with Imaging Appearances of Glioblastoma should be Managed as Glioblastoma.
• Hereditary cancer syndrome diagnosis: molecular genetic clues and cancer control.
• Large global effective population sizes in Paramecium.
• Nutrient signaling components controlling protein synthesis in striated muscle.
• Paraneoplastic anti-N-methyl-D-aspartate receptor encephalitis associated with ovarian teratoma.
• Pharmacological therapy for Wegener's granulomatosis.
• Presence or absence of lipopolysaccharide O antigens affects type III secretion by Pseudomonas aeruginosa.
• Rapamycin blunts nutrient stimulation of eIF4G, but not PKCepsilon phosphorylation, in skeletal muscle.
• Response to treatment and survival of patients with non-small cell lung cancer undergoing somatic EGFR mutation testing.
• Results from an autonomous underwater vehicle towed hydrophone array experiment in Nantucket Sound.
• Tantalus, a 240MeV Dedicated Source of Synchrotron Radiation, 1968-1986.
• The effect of maternal socio-economic status throughout the lifespan on infant birthweight.
• The relative roles of three DNA repair pathways in preventing Caenorhabditis elegans mutation accumulation.
• Toward a consensus in molecular diagnosis of hereditary nonpolyposis colorectal cancer (Lynch syndrome).
• Who should be sent for genetic testing in hereditary colorectal cancer syndromes?