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Sutton, M. D.

Publications and source records attributed to Sutton, M. D..

2 recordsLinked to original sources

On the relationship between spatial environmental variability, dispersion and biodiversity

AimWe establish quantitative relationships between species richness and the rate of spatial change in controlled, digital, environments. We use a simplified, first-principles, stochastic, evolutionary model in which artificial organisms can evolve and disperse. We develop an understanding of how environmental variability in space influences species richness and how it is affected by organisms ability to disperse. Time periodAt each time step of the experiment, each organism can reproduce sexually, disperse and die. Each experiment is run for 100,000 time steps. The life span of each organism is 15 time steps. LocationThe model uses an artificial, digital, landscape consisting of a uniform (x, y) grid of cells, with a single environmental variable that changes sinusoidally in the x direction. Major taxa studiedOrganisms are defined by a 64-bit genome and reproduce sexually. These digital organisms are designed to mimic the basic principles of biological evolution. MethodsEach experiment starts with a single organism, which can mutate and reproduce sexually, producing offspring that can do all of the above and disperse in the environment. Monte Carlo experimentation is used to generate statistical insight into species richness by producing thousands of replicate simulations. ResultsA strong correlation is observed between mean species richness and the rate of spatial change in the environmental variable. This relationship holds true for a wide range of dispersal abilities, but diminishes when dispersal ability is very low. Main ConclusionsWe predict that the rate of change of environmental variables (e.g. the derivative of elevation) is a driver of real-world biodiversity where dispersal is sufficient. Our results suggest that the ability of organisms to disperse plays an important role in determining how biodiversity responds to environmental gradients.

ecology↗

Msh2-Msh3 interferes with DNA metabolism in vivo

Mismatch repair (MMR) is a highly conserved DNA repair pathway that safeguards the genome from errors in DNA replication. In Saccharomyces cerevisiae, two MutS homolog (Msh) complexes, Msh2-Msh3 or Msh2-Msh6, initiate MMR. Msh2-Msh3, the focus of this study, recognizes and directs repair of insertion/deletion loops (IDLs) up to ~17 nucleotides. Msh2-Msh3 also recognizes and binds distinct looped and branched DNA structures with varying affinities, thereby contributing to genome stability outside post-replicative MMR through homologous recombination, double-strand break repair (DSBR), and the DNA damage response. Msh2-Msh3 also promotes genome instability through trinucleotide repeat (TNR) expansions. This non-canonical activity is likely an unfortunate consequence of Msh2-Msh3s intrinsic ability to bind a wide range of DNA structures, including those formed with single-stranded (ss) TNR sequences. We previously demonstrated that Msh2-Msh3 binding to 5 ssDNA flap structures interfered with the in vitro binding and cleavage activities of the flap endonuclease Rad27 (Fen1 in mammals), which promotes 5 ssDNA flap processing during Okazaki fragment maturation (OFM) and long-patch base excision repair (LP-BER). Here we demonstrate that elevated Msh2-Msh3 levels interfere with DNA replication and LP-BER in vivo, consistent with the hypothesis that protein abundance and Msh3 ATPase activities are key drivers of Msh2-Msh3-mediated genomic instability.

genetics↗