Biomedical subjects

Root Gorelick

Publications and source records attributed to Root Gorelick.

4 recordsLinked to original sources

PubMed2004

Normalized mutual entropy in biology: quantifying division of labor.

Division of labor is one of the primary adaptations of sociality and the focus of much theoretical work on self-organization. This work has been hampered by the lack of a quantitative measure of division of labor that can be applied across systems. We divide Shannon's mutual entropy by marginal entropy to quantify division of labor, rendering it robust over changes in number of individuals or tasks. Reinterpreting individuals and tasks makes this methodology applicable to a wide range of other contexts, such as breeding systems and predator-prey interactions.

Animals↗

PubMed2004

Neo-Lamarckian medicine.

Darwinian medicine is the treatment of disease based on evolution. The underlying assumption of Darwinian medicine is that traits are coded by genes, which are often assumed to be sequences of DNA nucleotides. The quantitative genetic ramification of this perspective is that traits, including disease susceptibility, are either caused by genes or by the environment, with genotype-by-environment interactions usually considered statistical artefacts. I emphasize also examining those epigenetic signals that can be altered by environmental perturbations and then transmitted to subsequent generations. Although seldom studied, environmentally-alterable meiotically-heritable epigenetic signals exist and provide a mechanism underlying genotype-by-environment interactions. Environment of a parent can affect its descendants by heritably altering epigenetic signals. Neo-Lamarckian medicine is the application of these evolutionary epigenetic notions to diseases and could have enormous public health and environmental policy implications. If industrial contaminants adversely affect organisms by meiotically-heritably altering their epigenetic signals, then cleaning up these contaminants will not remedy the problem. Once contaminants have adversely altered an individual's epigenetic signals, this harm will be transmitted to future generations even if they are not exposed to the contaminant. Exposure to environmental shocks such as free radicals or other carcinogens can alter cytosine methylation patterns on regulatory genes. This can cause cancer by up-regulating genes for cell division or by down-regulating tumour suppressor genes. Environmentally-alterable meiotically-heritable epigenetic signals could also underlie other diseases, such as diabetes, Prader-Willi syndrome, and many complex diseases. If environmentally-altered meiotically-heritable epigenetic effects are widespread - which is an important open empirical question - they have the potential to alter paradigmatic views of evolutionary medicine and the putative dichotomy of nature versus nurture. Neo-Lamarckian medicine would thereby shift emphasis from cure to prevention of diseases.

Animals↗

PubMed2004

Decomposing multilocus linkage disequilibrium.

We present a mathematically precise formulation of total linkage disequilibrium between multiple loci as the deviation from probabilistic independence and provide explicit formulas for all higher-order terms of linkage disequilibrium, thereby combining J. Dausset et al.'s 1978 definition of linkage disequilibrium with H. Geiringer's 1944 approach. We recursively decompose higher-order linkage disequilibrium terms into lower-order ones. Our greatest simplification comes from defining linkage disequilibrium at a single locus as allele frequency at that locus. At each level, decomposition of linkage disequilibrium is mathematically equivalent to number theoretic compositions of positive integers; i.e., we have converted a genetic decomposition into a mathematical decomposition.

Alleles↗

PubMed2003

Colony response to graded resource changes: an analytical model of the influence of genotype, environment, and dominance.

Successful social groups must respond dynamically to environmental changes. However, a flexible group response requires the coordination of many individuals. Here we offer a static analytical model that integrates variation in environment-based cues for performance of a task with genetically and environmentally based variation in individual responses, and predicts the resultant colony behavior for that task. We also provide formulae for computing effective number of alleles in a haplo-diploid colony founded by any number of parents. Variable colony resources combined with variation among worker phenotypes generate known patterns of colony flexibility, allowing us to explicitly test how the number of loci, dominance/codominance, and the phenotype's environment influences group response. Our model indicates that the number of loci strongly influences colony behavior. For one or two loci, the proportion of workers foraging for pollen remain constant over vast increases in colony pollen stores, but then drops dramatically when the pollen stores increase past a specific threshold. As the number of loci controlling pollen foraging increases, graded increases in pollen stores result in a graded drop in the proportion of the worker population foraging for pollen. The effect of number of alleles is less strong, a result we discuss in light of the fact that a low number of effective alleles are expected in a colony. Comparisons of our model with empirical honey bee (Apis mellifera) data indicate that worker foraging response to pollen stores is driven by one or two loci, each with dominant allelic effects. The growing body of evidence that genotype has strong effects on task performance in social insect colonies, and the variation in within-colony genetic diversity across social insect taxa, make our model broadly applicable in explaining social group coordination.

Alleles↗