Polydomy in ants: what we know, what we think we know, and what remains to be done

The correct identification of colony boundaries is an essential prerequisite for empirical studies of ant behaviour and evolution. Ant colonies function at various organizational levels, and these boundaries may be difficult to assess. Moreover, new complexity can be generated through the presence of spatially discrete subgroups within a more or less genetically homogeneous colony, a situation called polydomy. A colony is polydomous only if individuals (workers and brood) of its constituent nests function as a social and cooperative unit and are regularly interchanged among nests. This condition was previously called polycalic, and the term polydomy was used in a broader sense for a group of daughter nests of the same mother colony (implying limited female dispersal), without regard to whether these different nests continued to exchange individuals. We think that this distinction between ‘polycaly’ and ‘polydomy’ concerns two disparate concepts. We thus prefer the narrower definition of polydomy, which groups individuals that interact socially. Does this new level of organization affect the way in which natural selection acts on social traits? Here, after examining the history of terms, we review all ant species that have been described as expressing polydomous structures. We show that there is no particular syndrome of traits predictably associated with polydomy. We detail the existing theoretical predictions and empirical results on the ecology of polydomy, and the impact of polydomy on social evolution and investment strategies, while carefully distinguishing monogynous from polygynous species. Finally, we propose a methodology for future studies and offer ideas about what remains to be done. © 2007 The Linnean Society of London, Biological Journal of the Linnean Society, 2007, 90 , 319–348.     

Changing the way we think about global change research: scaling up in experimental ecosystem science

Scaling is a naturally iterative and bi‐directional component of problem solving in ecology and in climate science. Ecosystems and climate systems are unquestionably the sum of all their parts, to the smallest imaginable scale, in genomic processes or in the laws of fluid dynamics. However, in the process of scaling‐up, for practical purposes thewhole usually has to be construed as a good deal less than this. This essay demonstrates how controlled large‐scale experiments can be used to deduce key mechanisms and thereby reduce much of the detail needed for the process of scaling‐up. Collection of the relevant experimental evidence depends on controlling the environment and complexity of experiments, and on applications of technologies that report on, and integrate, small‐scale processes. As the role of biological feedbacks in the behavior of climate systems is better appreciated, so the need grows for experimentally based understanding of ecosystem processes. We argue that we cannot continue as we are doing, simply observing the progress of the greenhouse gas‐driven experiment in global change, and modeling its future outcomes. We have to change the way we think about climate system and ecosystem science, and in the process move to experimental modes at larger scales than previously thought achievable.     

Richard J. Hobbs: how one ecologist has influenced the way we think about restoration ecology

Professor Richard Hobbs has had a profound influence on the development of the discipline of restoration ecology. With more than 300 publications spanning a broad scope of applied ecological sciences, he has collaborated with hundreds of researchers. His sometimes‐provocative insights, balanced by extensive empirical research, will have a lasting impact by encouraging people to think more broadly about the science and practice of ecological restoration. Here, on the eve of his retirement, some of his staff and students, past and present, take a retrospective look at his contributions to restoration ecology both as a scientist and as a mentor.     

More damaging than we think: Systemic effects of intestinal inflammation

Comment on: Westbrook AM, et al. Intestinal mucosal inflammation leads to systemic genotoxicity in mice. Cancer Res 2009; 69:4827-34.     

What strikes most when we think of Geoff

Purinergic Signalling -     

Metaphors we think with: the role of metaphor in reasoning

The way we talk about complex and abstract ideas is suffused with metaphor. In five experiments, we explore how these metaphors influence the way that we reason about complex issues and forage for further information about them. We find that even the subtlest instantiation of a metaphor (via a single word) can have a powerful influence over how people attempt to solve social problems like crime and how they gather information to make "well-informed" decisions. Interestingly, we find that the influence of the metaphorical framing effect is covert: people do not recognize metaphors as influential in their decisions; instead they point to more "substantive" (often numerical) information as the motivation for their problem-solving decision. Metaphors in language appear to instantiate frame-consistent knowledge structures and invite structurally consistent inferences. Far from being mere rhetorical flourishes, metaphors have profound influences on how we conceptualize and act with respect to important societal issues. We find that exposure to even a single metaphor can induce substantial differences in opinion about how to solve social problems: differences that are larger, for example, than pre-existing differences in opinion between Democrats and Republicans.     

The wrong way to think about gene conversion?

Summary The sex circle model for crossing over and gene conversion proposed by Stahl has a number of properties which are in conflict with a considerable body of recombination data in fungi. The model is unable to explain the observed frequencies of gene conversion and postmeiotic segregation for particular mutants in several species. It does not provide an explanation for fine structure map expansion, nor does it account satisfactorily for the polarised distribution of outside markers amongst allelic recombinants.     

Thermometers: something for statistical geneticists to think about

In human genetics, we measure the strength of statistical evidence using a variety of maximized likelihood ratios, LODs, and empirical p values. I argue here that these statistics have highly undesirable properties as evidence measures when applied to complex disorders. Among other deficiencies, I show that when following up on an interesting finding, they will tend to erroneously indicate diminished evidence as more data are considered (e.g., the LOD will tend to go down at a linked locus as the sample size increases). This violates a fundamental assumption underlying standard linkage and association designs in which we first scan the genome for our best signals, and then follow up at those genomic positions with additional data. I argue here for a coherent theoretical approach to formalizing statistical evidence measures, and derive a set of minimal requirements that any evidence measure should meet, drawing heavily on an analogy with the thermometer. I speculate that measures of evidence that come closer to meeting these requirements will do a better job of finding and characterizing genes, and I propose an alternative evidence metric as a step in this direction.     

What we talk about when we talk about access deficits

Semantic impairments have been divided into storage deficits, in which the semantic representations themselves are damaged, and access deficits, in which the representations are intact but access to them is impaired. The behavioural phenomena that have been associated with access deficits include sensitivity to cueing, sensitivity to presentation rate, performance inconsistency, negative serial position effects, sensitivity to number and strength of competitors, semantic blocking effects, disordered selection between strong and weak competitors, correlation between semantic deficits and executive function deficits and reduced word frequency effects. Four general accounts have been proposed for different subsets of these phenomena: abnormal refractoriness, too much activation, impaired competitive selection and deficits of semantic control. A combination of abnormal refractoriness and impaired competitive selection can account for most of the behavioural phenomena, but there remain several open questions. In particular, it remains unclear whether access deficits represent a single syndrome, a syndrome with multiple subtypes or a variable collection of phenomena, whether the underlying deficit is domain-general or domain-specific, whether it is owing to disorders of inhibition, activation or selection, and the nature of the connection (if any) between access phenomena in aphasia and in neurologically intact controls. Computational models offer a promising approach to answering these questions.