How can automimicry persist when predators can preferentially consume undefended mimics?

It is common for species that possess toxins or other defences to advertise these defences to potential predators using aposematic ("warning") signals. There is increasing evidence that within such species, there are individuals that have reduced or non-existent levels of defence but still signal. This phenomenon (generally called automimicry) has been a challenge to evolutionary biologists because of the need to explain why undefended automimics do not gain such as a fitness advantage by saving the physiological costs of defence that they increase in prevalence within the population, hence making the aposematic signal unreliable. The leading theory is that aposematic signals do not stop all predatory attacks but rather encourage predators to attack cautiously until they have identified the defence level of a specific individual. They can then reject defended individuals and consume the undefended. This theory has recently received strong empirical support, demonstrating that high-accuracy discrimination appears possible. However, this raises a new evolutionary problem: if predators can perfectly discriminate the defended from the undefended and preferentially consume the latter, then how can automimicry persist? Here, we present four different mechanisms that can allow non-trivial levels of automimics to be retained within a population, even in the extreme case where predators can differentiate defended from undefended individuals with 100% accuracy. These involve opportunity costs to the predator of sampling carefully, temporal fluctuation in predation pressure, predation pressure being correlated with the prevalence of automimicry, or developmental or evolutionary constraints on the availability of defence. These mechanisms generate predictions as to the conditions where we would expect aposematically signalling populations to feature automimicry and those where we would not.     

What can we teach Lymnaea and what can Lymnaea teach us?

This review describes the advantages of adopting a molluscan complementary model, the freshwater snail Lymnaea stagnalis, to study the neural basis of learning and memory in appetitive and avoidance classical conditioning; as well as operant conditioning of its aerial respiratory and escape behaviour. We firstly explored ‘what we can teach Lymnaea’ by discussing a variety of sensitive, solid, easily reproducible and simple behavioural tests that have been used to uncover the memory abilities of this model system. Answering this question will allow us to open new frontiers in neuroscience and behavioural research to enhance our understanding of how the nervous system mediates learning and memory. In fact, from a translational perspective, Lymnaea and its nervous system can help to understand the neural transformation pathways from behavioural output to sensory coding in more complex systems like the mammalian brain. Moving on to the second question: ‘what can Lymnaea teach us?’, it is now known that Lymnaea shares important associative learning characteristics with vertebrates, including stimulus generalization, generalization of extinction and discriminative learning, opening the possibility to use snails as animal models for neuroscience translational research.     

What can we teach Drosophila? What can they teach us?

A number of single gene mutations dramatically reduce the ability of fruit flies to learn or to remember. Cloning of the affected genes implicated the adenylyl cyclase second-messenger system as key in learning and memory. The expression patterns of these genes, in combination with other data, indicates that brain structures called mushroom bodies are crucial for olfactory learning. However, the mushroom bodies are not dedicated solely to olfactory processing; they also mediate higher cognitive functions in the fly, such as visual context generalization. Molecular genetic manipulations, coupled with behavioral studies of the fly, will identify rudimentary neural circuits that underly multisensory learning and perhaps also the circuits that mediate more-complex brain functions, such as attention.     

What can we teach Drosophila? What can they teach us?

A number of single gene mutations dramatically reduce the ability of fruit flies to learn or to remember. Cloning of the affected genes implicated the adenylyl cyclase second-messenger system as key in learning and memory. The expression patterns of these genes, in combination with other data, indicates that brain structures called mushroom bodies are crucial for olfactory learning. However, the mushroom bodies are not dedicated solely to olfactory processing; they also mediate higher cognitive functions in the fly, such as visual context generalization. Molecular genetic manipulations, coupled with behavioral studies of the fly, will identify rudimentary neural circuits that underly multisensory learning and perhaps also the circuits that mediate more-complex brain functions, such as attention.     

When can dispersal synchronize populations?

While spatial synchrony of oscillating populations has been observed in many ecological systems, the causes of this phenomenon are still not well understood. The most common explanations have been the Moran effect (synchronous external stochastic influences) and the effect of dispersal among populations. Since ecological systems are typically subject to large spatially varying perturbations which destroy synchrony, a plausible mechanism explaining synchrony must produce rapid convergence to synchrony. We analyze the dynamics through time of the synchronizing effects of dispersal and, consequently, determine whether dispersal can be the mechanism which produces synchrony. Specifically, using methods new to ecology, we analyze a two patch predator-prey model, with identical weak dispersal between the patches. We find that a difference in time scales (i.e. one population has dynamics occurring much faster than the other) between the predator and prey species is the most important requirement for fast convergence to synchrony.     

Microvinification--how small can we go?

High-throughput methodologies to screen large numbers of microorganisms necessitate the use of small-scale culture vessels. In this context, an increasing number of researchers are turning to microtiter plate (MTP) formats to conduct experiments. MTPs are now widely used as a culturing vessel for phenotypic screening of aerobic laboratory cultures, and their suitability has been assessed for a range of applications. The work presented here extends these previous studies by assessing the metabolic footprint of MTP fermentation. A comparison of Chardonnay grape juice fermentation in MTPs with fermentations performed in air-locked (self-induced anaerobic) and cotton-plugged (aerobic) flasks was made. Maximum growth rates and biomass accumulation of yeast cultures grown in MTPs were indistinguishable from self-induced anaerobic flask cultures. Metabolic profiles measured differed depending on the metabolite. While glycerol and acetate accumulation mirrored that of self-induced anaerobic cultures, ethanol accumulation in MTP ferments was limited by the increased propensity of this volatile metabolite for evaporation in microlitre-scale culture format. The data illustrates that microplate cultures can be used as a replacement for self-induced anaerobic flasks in some instances and provide a useful and economical platform for the screening of industrial strains and culture media.     

How weird can mimicry get?

Classical mimicry theory distinguishes clearly between the mutualistic resemblance between two or more defended species (muellerian mimicry), and the parasitic resemblance of a palatable species to a defended species (batesian mimicry). Modelling the behaviour of predators, without initially taking ecological complications into account, is a good strategy for exploring whether this division is valid. Two such behavioural models are described: conditioning theory, which simulates changes in motivational attack levels according to the norms of current learning theory; and saturation theory, which considers how a predator may become saturated with a particular toxic compound, and then cease feeding on the prey species that delivers it. This effect is to be clearly distinguished from simple satiation. Most formulations of the conditioning model allow the direction of reinforcement produced by a particular prey to change according the predator's current state of motivation: this leads to the existence of quasi-batesian mimicry, a parasitic mimicry between two species that could both be described as defended. At high densities, two prey species that share a chemical defense will be ‘muellerian mutualists’, mutually protecting each other against predators that have been saturated with the defensive compound. This mutualism may be accompanied by true muellerian mimicry of the colour patterns, or the patterns may be completely different. This can therefore be regarded as a form of mimicry in a non-visual communication channel. Even an apparently palatable prey species may be effectively unavailable to predators if its density is such as to deliver a particular nutrient in excess of the predator's need for a balanced diet. Such a nutrient in effect becomes a toxin, and such an abundant prey species would be partly defended and potentially able to act as the model in a mimicry system. Thus there might be protective mimicry between ‘palatable’ species, and a ‘palatable’ species might even function as the model for a ‘defended’ mimic. These unorthodox kinds of mimicry probably exist transiently during fluctuations of prey populations. It is less likely that these conditions persist for long enough to induce the evolution of mimicry, and the relationships perhaps usually occur when mimicry already exists for other reasons. Mimicry rings may be mutually stabilised by a combination of toxic mutualism and the exchange of species between the rings. Colour polymorphism in a defended species is strictly neutral whenever the population is dense enough to saturate the predator. This, as well as quasi-batesian mimicry, may help to explain the minority of warningly coloured species that are polymorphic. This revised version was published online in July 2006 with corrections to the Cover Date.     

How much pollen can thrips destroy?

ABSTRACT. 1. A laboratory technique for measuring the number of pollen grains consumed by thrips is described.
2. Thrips imaginis Bagnall and Thrips obscuratus (Crawford) (Thripidae) were studied particularly on pollen of the kiwifruit Actinidia deliciosa (A. Chevalier) Liang & Ferguson in New Zealand, and Echium plantagineum L. in Australia.
3. Mean daily feeding rates (in grains per thrips per day) ranged from 29 to 843, with an individual rate as high as 1626 for T.imaginis larvae II on E. plantagineum.
4. The time taken to feed on a single grain was proportional to grain volume, and decreased with temperature.
5. Daily feeding rates were significantly different between pollens, and were higher for smaller grains. The total volume of pollen contents consumed and the total time spent ingesting this volume per thrips per day may be constant with respect to pollen species.
6. Daily feeding rates were equivalent to 0.2–0.7% of the average total pollen production of a flower per thrips per day.
7. Extrapolation of the daily feeding rates suggests that pollen damage by thrips could sometimes be reducing crop yield or plant fitness.     

What can we do about osteoarthritis?

Osteoarthritis is complex in genetics, pathogenesis, monitoring and treatment. Current treatment of osteoarthritis does not influence progression. Much could be gained by more effective 'low-tech-low-cost' treatment. However, many patients have rapidly progressive disease, multiple joint involvement, and severe disease. We need to clarify the genetics of osteoarthritis, identify those at risk for progression and severe disease, and identify molecular processes critical for joint survival and failure. Will saving the cartilage improve patient pain and function? Effective outcome measures are needed to accelerate testing of new treatments. Further improvement is needed in joint implant technology to decrease costs, wear and loosening.     

What can microbial genetics teach sociobiology?

Progress in our understanding of sociobiology has occurred with little knowledge of the genetic mechanisms that underlie social traits. However, several recent studies have described microbial genes that affect social traits, thereby bringing genetics to sociobiology. A key finding is that simple genetic changes can have marked social consequences, and mutations that affect cheating and recognition behaviors have been discovered. The study of these mutants confirms a central theoretical prediction of social evolution: that genetic relatedness promotes cooperation. Microbial genetics also provides an important new perspective: that the genome-to-phenome mapping of social organisms might be organized to constrain the evolution of social cheaters. This constraint can occur both through pleiotropic genes that link cheating to a personal cost and through the existence of phoenix genes, which rescue cooperative systems from selfish and destructive strategies. These new insights show the power of studying microorganisms to improve our understanding of the evolution of cooperation.     

What can epigenomics do for you?

Genome-wide 5-hydroxymethylome analysis of a rodent hepatocarcinogen model reveals that 5-hydroxymethylcytosine-dependent active DNA demethylation may be functionally important in the early stages of carcinogenesis. See research article http://genomebiology.com/2012/13/10/R93     

What can GPI do for you?

Various functions for glycosylphosphatidylinositol (GPI) protein anchors have been described in mammalian and protozoan systems. These data suggest that some functions are common to higher and lower eukaryotes, whereas others may represent adaptations that are specifically advantageous to either unicellular or metazoan organisms. In this article, Mike Ferguson discusses the current theories of GPI function that have relevance to protozoan parasites and their mammalian hosts.