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Exchange Events (exchange + event)

Distribution by Scientific Domains

Life Sciences	60%

Selected Abstracts

Genetic transduction in freshwater ecosystems

FRESHWATER BIOLOGY, Issue 6 2008
OLADELE A. OGUNSEITAN
Summary 1. Lateral genetic exchange is a profound consequence of the co-existence of viruses (bacteriophages) and bacteria in freshwater ecosystems. Transduction is distinct from other mechanisms of genetic exchange because it is driven by potentially lethal agents external to the donor and recipient cells. Therefore, transduction is reputed to be a major driving force behind the diversity in natural populations and communities of bacteria. 2. Both generalized transduction (where every segment of the donor's genome has equal chance of being transferred to a recipient cell) and specialized transduction (where certain donor gene sequences are transferred at higher frequencies than others based on their proximity to the integration site of the transducing bacteriophage genome) have been demonstrated for various freshwater bacteria. However, these genetic exchange events occur at frequencies that vary widely, from 10,2 to 10,10 transductants per recipient, depending on the influence of various physical, chemical and biotic environmental factors on the outcome of phage,host encounters. Methodological constraints limit the interpretation of results from early studies of transduction in freshwaters because those studies introduced exogenous organisms in microcosms and excluded, to different extents, naturally occurring environmental conditions and their variability. 3. To assist the design and extrapolation of empirical observations, mathematical models including application of Group Theory are useful to estimate boundaries of the impact of transduction in generating and maintaining microbial diversity in freshwater. These theoretical excursions generate hypotheses and questions that can only be answered through refinement of current empirical estimates of transduction frequency, polarity of gene mobilization, bacteriophage host ranges, and the influence of gradients in environmental parameters that characterize freshwater ecosystems. [source]

Quantification of sequence exchange events between PMS2 and PMS2CL provides a basis for improved mutation scanning of lynch syndrome patients,

HUMAN MUTATION, Issue 5 2010
Heleen M. van der Klift
Abstract Heterozygous mutations in PMS2 are involved in Lynch syndrome, whereas biallelic mutations are found in Constitutional mismatch repair-deficiency syndrome patients. Mutation detection is complicated by the occurrence of sequence exchange events between the duplicated regions of PMS2 and PMS2CL. We investigated the frequency of such events with a nonspecific polymerase chain reaction (PCR) strategy, coamplifying both PMS2 and PMS2CL sequences. This allowed us to score ratios between gene and pseudogene-specific nucleotides at 29 PSV sites from exon 11 to the end of the gene. We found sequence transfer at all investigated PSVs from intron 12 to the 3, end of the gene in 4 to 52% of DNA samples. Overall, sequence exchange between PMS2 and PMS2CL was observed in 69% (83/120) of individuals. We demonstrate that mutation scanning with PMS2 -specific PCR primers and MLPA probes, designed on PSVs, in the 3, duplicated region is unreliable, and present an RNA-based mutation detection strategy to improve reliability. Using this strategy, we found 19 different putative pathogenic PMS2 mutations. Four of these (21%) are lying in the region with frequent sequence transfer and are missed or called incorrectly as homozygous with several PSV-based mutation detection methods. Hum Mutat 31:578,587, 2010. © 2010 Wiley-Liss, Inc. [source]

Temperature dependence of structure and dynamics of the hydrated Ca2+ ion according to ab initio quantum mechanical charge field and classical molecular dynamics

JOURNAL OF COMPUTATIONAL CHEMISTRY, Issue 6 2010
Len Herald V. Lim
Abstract Simulations using ab initio quantum mechanical charge field molecular dynamics (QMCF MD) and classical molecular dynamics using two-body and three-body potentials were performed to investigate the hydration of the Ca2+ ion at different temperatures. Results from the simulations demonstrate significant effects of temperature on solution dynamics and the corresponding composition and structure of hydrated Ca2+. Substantial increase in ligand exchange events was observed in going from 273.15 K to 368.15 K, resulting in a redistribution of coordination numbers to lower values. The effect of temperature is also visible in a red-shift of the ion-oxygen stretching frequencies, reflecting weakened ligand binding. Even the moderate increase from ambient to body temperature leads to significant changes in the properties of Ca2+ in aqueous environment. © 2009 Wiley Periodicals, Inc. J Comput Chem, 2010 [source]

Genetic instabilities of (CCTG)·(CAGG) and (ATTCT)·(AGAAT) disease-associated repeats reveal multiple pathways for repeat deletion

MOLECULAR CARCINOGENESIS, Issue 4 2009
Sharon F. Edwards
Abstract The DNA repeats (CTG)·(CAG), (CGG)·(CCG), (GAA)·(TTC), (ATTCT)·(AGAAT), and (CCTG)·(CAGG), undergo expansion in humans leading to neurodegenerative disease. A genetic assay for repeat instability has revealed that the activities of RecA and RecB during replication restart are involved in a high rate of deletion of (CTG)·(CAG) repeats in E. coli. This assay has been applied to (CCTG)·(CAGG) repeats associated with myotonic dystrophy type 2 (DM2) that expand to 11,000 copies and to spinocerebellar ataxia type 10 (SCA10) (ATTCT)·(AGAAT) repeats that expand to 4500 copies in affected individuals. DM2 (CCTG)·(CAGG) repeats show a moderate rate of instability, less than that observed for the myotonic dystrophy type 1 (CTG)·(CAG) repeats, while the SCA10 (ATTCT)·(AGAAT) repeats were remarkably stable in E. coli. In contrast to (CTG)·(CAG) repeats, deletions of the DM2 and SCA10 repeats were not dependent on RecA and RecB, suggesting that replication restart may not be a predominant mechanism by which these repeats undergo deletion. These results suggest that different molecular mechanisms, or pathways, are responsible for the instability of different disease-associated DNA repeats in E. coli. These pathways involve simple replication slippage and various sister strand exchange events leading to deletions or expansions, often associated with plasmid dimerization. The differences in the mechanisms of repeat deletion may result from the differential propensity of these repeats to form various DNA secondary structures and their differential proclivity for primer,template misalignment during replication. © 2009 Wiley-Liss, Inc. [source]