What does Drosophila genetics tell us about speciation?

Studies of hybrid inviability, sterility and 'speciation genes' in Drosophila have given insight into the genetic changes that result in reproductive isolation. Here, I survey some extraordinary and important advances in Drosophila speciation research. However, 'reproductive isolation' is not the same as 'speciation', and this Drosophila work has resulted in a lopsided view of speciation. In particular, Drosophila are not always well-suited to investigating ecological and other selection-driven primary causes of speciation in nature. Recent advances have made use of far less tractable, but more charismatic organisms, such as flowering plants, vertebrates and larger insects. Work with these organisms has complemented Drosophila studies of hybrid unfitness to provide a more complete understanding of speciation.     

What can yeast tell us about N-linked glycosylation in the Golgi apparatus?

The N-glycans found on eukaryotic glycoproteins occur in a vast range of different structures. A universal N-glycan core is attached to proteins during synthesis in the endoplasmic reticulum, and then diversity is generated as the proteins pass through the Golgi apparatus. Many of the Golgi-localised glycosyltransferases have now been identified in both yeast and mammalian cells, but it is still unclear how these enzymes are integrated into the Golgi and the rest of the cell so as to ensure efficient and specific processing of passing substrates. This review discusses the potential of the yeast system to address these issues.     

What can Caenorhabditis elegans tell us about the nuclear envelope?

The nuclear envelope (NE) of the eukaryotic cell provides an essential barrier that separates the nuclear compartment from the cytoplasm. In addition, the NE is involved in essential functions such as nuclear stability, regulation of gene expression, centrosome separation and nuclear migration and positioning. In metazoa the NE breaks down and re-assembles around the segregated chromatids during each cell division. In this review we discuss the molecular constituents of the Caenorhabditis elegans NE and describe their role in post-mitotic NE re-formation, as well as the usefulness of C. elegans as an in vivo system for analyzing NE dynamics.     

What can dolphins tell us about primate evolution?

Fifty-five million years ago, a furry, hoofed mammal about the size of a dog ventured into the shallow brackish remnant of the Tethys Sea and set its descendants on a path that would lead to their complete abandonment of the land. These early ancestors of cetaceans (dolphins, porpoises, and whales) thereafter set on an evolutionary course that is arguably the most unusual of any mammal that ever lived. Primates and cetaceans, because of their adaptation to exclusively different physical environments, have had essentially nothing to do with each other throughout their evolution as distinct orders. In fact, the closest phylogenetic relatives of cetaceans are even-toed ungulates.     

What can two-dimensional NMR tell us about proteins?

As a result of spectacular advances in recent years, nuclear magnetic resonance (NMR) is now firmly established as an essential tool in protein research, providing both a unique method for three-dimensional structure determination and powerful new approaches for studies of protein dynamics and folding.     

What can genetics tell us about population connectivity?

Genetic data are often used to assess ‘population connectivity’ because it is difficult to measure dispersal directly at large spatial scales. Genetic connectivity, however, depends primarily on the absolute number of dispersers among populations, whereas demographic connectivity depends on the relative contributions to population growth rates of dispersal vs. local recruitment (i.e. survival and reproduction of residents). Although many questions are best answered with data on genetic connectivity, genetic data alone provide little information on demographic connectivity. The importance of demographic connectivity is clear when the elimination of immigration results in a shift from stable or positive population growth to negative population growth. Otherwise, the amount of dispersal required for demographic connectivity depends on the context (e.g. conservation or harvest management), and even high dispersal rates may not indicate demographic interdependence. Therefore, it is risky to infer the importance of demographic connectivity without information on local demographic rates and how those rates vary over time. Genetic methods can provide insight on demographic connectivity when combined with these local demographic rates, data on movement behaviour, or estimates of reproductive success of immigrants and residents. We also consider the strengths and limitations of genetic measures of connectivity and discuss three concepts of genetic connectivity that depend upon the evolutionary criteria of interest: inbreeding connectivity, drift connectivity, and adaptive connectivity. To conclude, we describe alternative approaches for assessing population connectivity, highlighting the value of combining genetic data with capture‐mark‐recapture methods or other direct measures of movement to elucidate the complex role of dispersal in natural populations.     

What can DNA tell us about biological invasions?

It is often hoped that population genetics can answer questions about the demographic and geographic dynamics of recent biological invasions. Conversely, invasions with well-known histories are sometimes billed as opportunities to test methods of population genetic inference. In both cases, underappreciated limitations constrain the usefulness of genetic methods. The most significant is that human-caused invasions have occurred on historical timescales that are orders of magnitude smaller than the timescales of mutation and genetic drift for most multicellular organisms. Analyses based on the neutral theory of molecular evolution cannot resolve such rapid dynamics. Invasion histories cannot be reconstructed in the same way as biogeographic changes occurring over millenia. Analyses assuming equilibrium between mutation, drift, gene flow, and selection will rarely be applicable, and even methods designed for explicitly non-equilibrium questions often require longer timescales than the few generations of most invasions of current concern. We identified only a few population genetic questions that are tractable over such short timescales. These include comparison of alternative hypotheses for the geographic origin of an invasion, testing for bottlenecks, and hybridization between native and invasive species. When proposing population genetic analysis of a biological invasion, we recommend that biologists ask (i) whether the questions to be addressed will materially affect management practice or policy, and (ii) whether the proposed analyses can really be expected to address important population genetic questions. Despite our own enthusiasm for population genetic research, we conclude that genetic analysis of biological invasions is justified only under exceptional circumstances.     

What can patterns of differentiation across plant genomes tell us about adaptation and speciation?

Genome scans have become a common approach to identify genomic signatures of natural selection and reproductive isolation, as well as the genomic bases of ecologically relevant phenotypes, based on patterns of polymorphism and differentiation among populations or species. Here, we review the results of studies taking genome scan approaches in plants, consider the patterns of genomic differentiation documented and their possible causes, discuss the results in light of recent models of genomic differentiation during divergent adaptation and speciation, and consider assumptions and caveats in their interpretation. We find that genomic regions of high divergence generally appear quite small in comparisons of both closely and more distantly related populations, and for the most part, these differentiated regions are spread throughout the genome rather than strongly clustered. Thus, the genome scan approach appears well-suited for identifying genomic regions or even candidate genes that underlie adaptive divergence and/or reproductive barriers. We consider other methodologies that may be used in conjunction with genome scan approaches, and suggest further developments that would be valuable. These include broader use of sequence-based markers of known genomic location, greater attention to sampling strategies to make use of parallel environmental or phenotypic transitions, more integration with approaches such as quantitative trait loci mapping and measures of gene flow across the genome, and additional theoretical and simulation work on processes related to divergent adaptation and speciation.     

What can genetic variation tell us about the evolution of senescence?

Quantitative genetic approaches have been developed that allow researchers to determine which of two mechanisms, mutation accumulation (MA) or antagonistic pleiotropy (AP), best explain observed variation in patterns of senescence using classical quantitative genetic techniques. These include the creation of mutation accumulation lines, artificial selection experiments and the partitioning of genetic variances across age classes. This last strategy has received the lion''s share of empirical attention. Models predict that inbreeding depression (ID), dominance variance and the variance among inbred line means will all increase with age under MA but not under those forms of AP that generate marginal overdominance. Here, we show that these measures are not, in fact, diagnostic of MA versus AP. In particular, the assumptions about the value of genetic parameters in existing AP models may be rather narrow, and often violated in reality. We argue that whenever ageing-related AP loci contribute to segregating genetic variation, polymorphism at these loci will be enhanced by genetic effects that will also cause ID and dominance variance to increase with age, effects also expected under the MA model of senescence. We suggest that the tests that seek to identify the relative contributions of AP and MA to the evolution of ageing by partitioning genetic variance components are likely to be too conservative to be of general value.     

What else can green monkeys tell us about AIDS?

Although the development of an HIV vaccine may eventually provide a means of controlling AIDS in developed countries, more immediate and less sophisticated methods are going to have to be developed for use in the rural regions of Africa where AIDS may already have reached epidemic proportions. Evidence from several studies of wild primates suggests that plant secondary compounds may commonly act as control agents for a variety of different pathogens. Although studies of laboratory populations of green monkeys indicate that their resistance to AIDS is likely to be genetic, we argue that it may be worth screening some of the plants eaten by African primates in the hope of coming up with compounds that exhibit suitable anti-viral activity. Any compounds isolated in this way are likely to be much cheaper to manufacture than laboratory-produced drugs and may also have been already screened for unpleasant side-effects.     

What can mathematical modeling tell us about hybrid invasions?

Compared to the vast theoretical literature on the dynamics of single species invasions, relatively few models have dealt with the emergence of invasive hybrids. Here, we review the variety of modeling approaches that have been used to study the dynamics of hybridization, outlining the underlying assumptions and highlighting their advantages and disadvantages. We summarize the predicted outcomes for the persistence for the native species and the resulting genetic composition of the native–exotic–hybrid complex under a variety of model scenarios. We highlight promising future directions for theoretical investigation and its integration with experimental studies.     

What can rodent models tell us about cognitive decline in Alzheimer's disease?

The prolongation of life and the rapidly increasing incidence of Alzheimer's disease have brought to the foreground the need for greater understanding of the etiology of the disease and the means to prevent or at least slow down the process. Out of this need the transgenic mouse and the production of synthetic amyloid peptides have been developed in an attempt to create experimental models of Alzheimer's disease that will help our understanding of the cellular and molecular mechanisms by which the pathology leads to memory dysfunction and to test potential therapeutic strategies. Despite 10 or so years of reasonably intensive research with these models, both fall short of producing a viable and faithful model of the complete pathology of Alzheimer's disease and the behavioral consequences are far from modelling the progressive decline in cognitive function. Here we review the advantages and the caveats associated with the two models in terms of the pathology, the associated memory dysfunction, and the effect on synaptic plasticity. Given the more recent advances that have been made in the understanding of the neurobiological changes that occur with the disease and with the consideration of other environmental effects, which have been clearly shown to have an impact on the progression of the disease in humans, we emphasis the advantage of pharmacological or environmental in transgenic mice or rodents injected with synthetic peptides that may prove to be more fruitful in our understanding of the memory deficits associated with the disease.     

What can epidemiology tell us about risks at low doses?

Puskin, J. S. What Can Epidemiology Tell Us about Risks at Low Doses? Radiat. Res. 169, 122-124 (2008). Limitations on statistical power preclude direct detection and quantification of radiogenic cancer risks at very low (environmental) levels of low-LET radiation through epidemiological studies. Given this limitation and our incomplete understanding of cellular processes leading to radiation carcinogenesis, an "effective threshold" in the dose range of interest for radiation protection cannot yet be ruled out. Ongoing epidemiological studies of chronically exposed individuals receiving very low daily doses of radiation can be used, however, together with radiobiological data, to critically test whether such a threshold is plausible.