Indirect genetic effects and the genetic bases of social dominance: evidence from cattle

Genetic studies of social behaviour have currently received new impetus from models including indirect genetic effects (IGEs) of social partners. This study aimed at investigating the contribution of conspecifics in social dominance, considered as response of dyadic interaction that is, winning (dominant individual) or losing (subordinate). A genetic correlation of −1 is expected between the attitude to win and the attitude to loose, and because a population always accounts for half winners and half losers, the heritability of the dominant status should be close to zero. Specifically, social dominance was studied in Aosta Chestnut and Aosta Black Pied (Bos taurus) breeds, alpine rustic cattle famous for traditional tournaments where pairs of cows assess dominant status in bloodless fights. The outcomes of 25 590 dyadic interactions performed by 8159 individuals in 11 years were analysed by applying a classical quantitative model and models including indirect effects. Data were analysed via Bayesian approach on a threshold trait. The assessment of variances revealed a genetic correlation of −0.976 between direct and indirect genetic components. The heritability measured on a liability scale was 0.122 for direct phenotype, but decreased to 0.014 when the total heritable variance (TBV) was considered. The trend of estimated breeding values showed that the total TBV was constant over the years, even though its direct component increased and the indirect part decreased. This result confirms the relevance of IGEs on social behaviour and the assumption that the mean individual social dominance cannot evolve within a population, due to the evolutionary constraints imposed by the ‘social environment''.     

The probability of parallel genetic evolution from standing genetic variation

Parallel evolution is often assumed to result from repeated adaptation to novel, yet ecologically similar, environments. Here, we develop and analyse a mathematical model that predicts the probability of parallel genetic evolution from standing genetic variation as a function of the strength of phenotypic selection and constraints imposed by genetic architecture. Our results show that the probability of parallel genetic evolution increases with the strength of natural selection and effective population size and is particularly likely to occur for genes with large phenotypic effects. Building on these results, we develop a Bayesian framework for estimating the strength of parallel phenotypic selection from genetic data. Using extensive individual‐based simulations, we show that our estimator is robust across a wide range of genetic and evolutionary scenarios and provides a useful tool for rigorously testing the hypothesis that parallel genetic evolution is the result of adaptive evolution. An important result that emerges from our analyses is that existing studies of parallel genetic evolution frequently rely on data that is insufficient for distinguishing between adaptive evolution and neutral evolution driven by random genetic drift. Overcoming this challenge will require sampling more populations and the inclusion of larger numbers of loci.     

Protecting groups from genetic research

Genetics research, like research in sociology and anthropology, creates risks for groups from which research subjects are drawn. This paper considers what sort of protection for groups from the risks of genetics research should be provided and by whom. The paper categorizes harms by distinguishing process-related from outcome-related harms and by distinguishing two kinds of group harms. It argues that calls for community engagement are justified with respect to some kinds of harms, but not with respect to others; and it cautions that community engagement may itself be harmful.     

Adaptation from standing genetic variation

Populations adapt to novel environments in two distinct ways: selection on pre-existing genetic variation and selection on new mutations. These alternative sources of beneficial alleles can result in different evolutionary dynamics and distinct genetic outcomes. Compared with new mutations, adaptation from standing genetic variation is likely to lead to faster evolution, the fixation of more alleles of small effect and the spread of more recessive alleles. There is potential to distinguish between adaptation from standing variation and that from new mutations by differences in the genomic signature of selection. Here we review these approaches and possible examples of adaptation from standing variation in natural populations. Understanding how the source of genetic variation affects adaptation will be integral for predicting how populations will respond to changing environments.     

Reconstructing pathways in large genetic networks from genetic perturbations.

I present an algorithm that determines the longest path between every gene pair in an arbitrarily large genetic network from large scale gene perturbation data. The algorithm's computational complexity is O(nk(2)), where n is the number of genes in the network and k is the average number of genes affected by a genetic perturbation. The algorithm is able to distinguish a large fraction of direct regulatory interactions from indirect interactions, even if the accuracy of its input data is substantially compromised.     

Determining the genetic diversity of lactobacilli from the oral cavity

Several methods for determining the diversity of Lactobacillus spp were evaluated with the purpose of developing a realistic approach for further studies. The patient population was comprised of young children with an oral disease called severe early childhood caries. The ultimate goal of these studies was to ascertain the role of lactobacilli in the caries process. To accomplish that goal, we evaluated several methods and approaches for determining diversity including AP-PCR, chromosomal DNA fingerprinting, denaturing gradient gel electrophoresis, and 16S rRNA gene sequencing. Central to these methods was the gathering and screening of isolates from cultivation medium. Using various estimates of diversity, we addressed the question as to how many isolates represent the overall diversity and how cultivation compares to non-cultivation techniques. Finally, we proposed a working approach for achieving the goals outlined framed by both practical constraints in terms of time, effort and efficacy while yielding a reliable outcome.     

Population genetic structure of mussels from the Baltic Sea

In a macrogeographic survey, the population genetic structure of mussels from various regions of the Baltic Sea, a large semi-enclosed brackish-water basin, was examined with reference toMytilus edulis andM. galloprovincialis samples from the North Sea, Irish coast and southern Portugal. Electrophoretically detectable variation was analysed at 6 polymorphic enzyme loci (Ap, Est-D, Lap-2, Odh, Pgi andPgm). Evidence was provided of a remarkably large amount of biochemical genetic differentiation among ecologically and morphologically divergent mussel populations in the Baltic. Patterns of allele frequencies in low-salinity populations from the area of the Baltic Proper were demonstrated to be widely homogeneous but contrast strongly with those of the western Baltic, the latter resembling populations from marine habitats of the North Sea. Associated with a pronounced salinity gradient, the spatial heterogeneity in gene-pool structure is indicated by steep clines of allele frequency changes in the area of the eastern Danish isles. The adaptive significance of the observed allozymic variation is suggested. From genetic distance estimates, the subdivision of population structure is discussed in relation to the significant amount of differentiation detected withinMytilus populations to date and to the evolutionary time required for the divergence of Baltic mussel populations. The allozymic data provide evidence for the genetic distinctiveness of mussels from the low-salinity areas of the Baltic. Their position at the specific or subspecific level of classification requires further consideration.     

Perspectives on human genetic variation from the HapMap Project

The completion of the International HapMap Project marks the start of a new phase in human genetics. The aim of the project was to provide a resource that facilitates the design of efficient genome-wide association studies, through characterising patterns of genetic variation and linkage disequilibrium in a sample of 270 individuals across four geographical populations. In total, over one million SNPs have been typed across these genomes, providing an unprecedented view of human genetic diversity. In this review we focus on what the HapMap project has taught us about the structure of human genetic variation and the fundamental molecular and evolutionary processes that shape it.     

Haldane's sieve and adaptation from the standing genetic variation

We consider populations that adapt to a sudden environmental change by fixing alleles found at mutation-selection balance. In particular, we calculate probabilities of fixation for previously deleterious alleles, ignoring the input of new mutations. We find that "Haldane's sieve"--the bias against the establishment of recessive beneficial mutations--does not hold under these conditions. Instead probabilities of fixation are generally independent of dominance. We show that this result is robust to patterns of sex expression for both X-linked and autosomal loci. We further show that adaptive evolution is invariably slower at X-linked than autosomal loci when evolution begins from mutation-selection balance. This result differs from that obtained when adaptation uses new mutations, a finding that may have some bearing on recent attempts to distinguish between hitchhiking and background selection by contrasting the molecular population genetics of X-linked vs. autosomal loci. Last, we suggest a test to determine whether adaptation used new mutations or previously deleterious alleles from the standing genetic variation.     

Evolutionary deviations from the universal genetic code in ciliates

The review surveys the information, including the most recent data, on the evolution of genetic code in ciliates, which is among the few codes deviating from the universal one. We discuss the cases of recurrent, independently arising deviations from the assignments of standard codons of polypeptide chain termination in the mitochondrial and nuclear genomes of ciliates and some other protozoans. Possible molecular mechanisms are considered, which underlie deviations from standard termination code to coding glutamine (codon UAA and UAG) and cystein or tryptophane (codon UGA) in the nuclear genome. Critical analysis of the main hypotheses on the evolution of secondary deviations from the universal code in ciliates is presented.     

Computation of genetic contributions from pedigrees

Summary A simple procedure is outlined by which genetic contributions of individuals to later generations can be estimated. The method, which involves simple matrix operations, is well suited to automatic computation.     

Cell division from a genetic perspective

A novel view of the eukaryotic cell cycle is taking form as genetic strategies borrowed from investigations of microbial gene regulation and bacteriophage morphogenesis are being applied to the process of cell division. It is a genetic construct in which mutational lesions identify the primary events, thermolabile gene products reveal temporal order, mutant phenotypes yield pathways of causality, and regulatory events are localized within sequences of gene controlled steps.     

A genetic legacy from archaic Homo

The roles of fossil human populations in the origin of modern humans have been enigmatic. Earlier (archaic) human populations were biologically similar and were in recurrent temporal and geographic contact, making interbreeding between ancient populations likely. Regardless of the taxonomic status of these populations, adaptive alleles may have introgressed from archaic populations into modern humans. When an introgressed archaic allele has a selective advantage, even rare interbreeding can lead to its spread or fixation in later human populations. Several genetic loci are candidates for such introgression, including microcephalin, a gene influencing brain development. This example may suggest that the evolution of human cognition depended in part on the genetic legacy of archaic groups such as the Neanderthals.     

Fatty acid-binding proteins--insights from genetic manipulations

Fatty acid-binding proteins (FABPs) belong to the conserved multigene family of the intracellular lipid-binding proteins (iLBPs). These proteins are ubiquitously expressed in vertebrate tissues, with distinct expression patterns for the individual FABPs. Various functions have been proposed for these proteins, including the promotion of cellular uptake and transport of fatty acids, the targeting of fatty acids to specific metabolic pathways, and the participation in the regulation of gene expression and cell growth. Novel genetic tools that have become available in recent years, such as transgenic cell lines, animals, and knock-out mice, have provided the opportunity to test these concepts in physiological settings. Such studies have helped to define essential cellular functions of individual FABP-types or of combinations of several different FABPs. The deletion of particular FABP genes, however, has not led to gross phenotypical changes, most likely because of compensatory overexpression of other members of the iLBP gene family, or even of unrelated fatty acid transport proteins. This review summarizes the properties of the various FABPs expressed in mammalian tissues, and discusses the transgenic and ablation studies carried out to date in a functional context.