Host dispersal as the driver of parasite genetic structure: a paradigm lost?

Understanding traits influencing the distribution of genetic diversity has major ecological and evolutionary implications for host–parasite interactions. The genetic structure of parasites is expected to conform to that of their hosts, because host dispersal is generally assumed to drive parasite dispersal. Here, we used a meta‐analysis to test this paradigm and determine whether traits related to host dispersal correctly predict the spatial co‐distribution of host and parasite genetic variation. We compiled data from empirical work on local adaptation and host–parasite population genetic structure from a wide range of taxonomic groups. We found that genetic differentiation was significantly lower in parasites than in hosts, suggesting that dispersal may often be higher for parasites. A significant correlation in the pairwise genetic differentiation of hosts and parasites was evident, but surprisingly weak. These results were largely explained by parasite reproductive mode, the proportion of free‐living stages in the parasite life cycle and the geographical extent of the study; variables related to host dispersal were poor predictors of genetic patterns. Our results do not dispel the paradigm that parasite population genetic structure depends on host dispersal. Rather, we highlight that alternative factors are also important in driving the co‐distribution of host and parasite genetic variation.     

Gondwanan break-up: legacies of a lost world?

Fierce debate surrounds the history of organisms in the southern hemisphere; did Gondwanan break-up produce ocean barriers that imposed distribution patterns on phylogenies (vicariance)? Or have organisms modified their distributions through trans-oceanic dispersal? Recent advances in biogeographical theory suggest that the current focus on vicariance versus dispersal is too narrow because it ignores 'geodispersal' (i.e. expansion of species into areas when geographical barriers disappear), extinction and sampling errors. Geodispersal produces multiple, conflicting vicariance patterns, and extinction and sampling errors destroy vicariance patterns. This perspective suggests that it is more difficult to detect vicariance than trans-oceanic dispersal and that specialized methods must be applied if an unbiased understanding of southern hemisphere biogeography is to be achieved.     

Microarrays: lost in a storm of data?

Microarray expression profiling is instrumental to our understanding of the function of the genome. Resolution of functionally relevant expression patterns will require the analysis of large data sets compiled from multiple investigators. For this and other reasons, I argue that it is crucial for array data to be publicly shared in a format as close to the 'raw data' as possible. Issues such as protection of intellectual property, ensuring quality of the data, and the format and timing for sharing array data are also discussed.     

Impact of urea on water structure: a clue to its properties as a denaturant?

A new investigation of the structure of urea-water solutions at a mole ratio of 1 urea to 4 water molecules is described. Neutron diffraction is used in conjunction with isotope labelling on the water and urea hydrogen atoms and on the nitrogen atom of urea. The diffraction data are analysed using the empirical potential structure refinement procedure to yield a set of site-site radial distribution functions and spatial density functions that are consistent with the diffraction data. The results are discussed in relation to recent and past X-ray and neutron diffraction experiments and theoretical studies of this system. It is found that urea incorporates readily into water, forming pronounced hydrogen bonds with water at both the amine and carbonyl headgroups. In addition the urea also hydrogen bonds to itself, forming chains or clusters consisting of up to approximately 60 urea molecules in a cluster. There, is however, little or no evidence of urea segregating itself from water, in marked contrast to a recent study of the methanol-water system. This behaviour is discussed in the context of the great propensity of urea to effect protein denaturation.     

HasIxianthes (Scrophulariaceae) lost its special bee?

Ixianthes retzioides is a rare, moderately sized, shrub with large yellow flowers that are lined with glandular trichomes. Preliminary analysis indicates that the trichomes secrete a complex mixture of lipids. Floral morphology suggests thatIxianthes should be pollinated by a large oil-collecting bee, yet only one possible candidate,Rediviva gig, is known and it occurs outside of the distributional range ofIxianthes. Despite observations ofIxianthes at different sites in different years, no oil-collecting bee has been observed visiting the flowers. This together with low fruit and seed set at the main study site suggests thatIxianthes has lost, at least locally, its specialized pollinator. Plants are self-compatible and set a limited amount of seed as a result of visits by pollen-collecting bees.     

Citric acid as a siderophore of enterococci?

In the pool of 70 enterococcal strains of the genus Enterococcus 61.4% released citrate into the medium. This metabolite has occurred more frequently in E. faecium strains. There was no correlation between hydroxamate siderophores production and citrate releasing. Only nine (10, 3%) of 70 strains have used Fe3+-dicitrate complex as iron sources. Iron restricted condition causing moderate inhibition of growth have not increased citrate releasing. When iron deficiency has caused stronger growth inhibition, E. faecalis strains did not release citrate and E. faecium strains its smaller amounts. The resting cells grown in iron-restricted condition have incorporated 59Fe3+ complexed by citrate more active than cells grown in the medium with excess of iron. So, citrate has not been a siderophore in enterococci.     

Trichinella as a modulator of flu-induced pathology?

In Trichinella spiralis and influenza co-infected mice, the influenza virus-induced secretion of the lung-damaging tumour necrosis factor alpha is modulated, as described by Furze et al. in a recent study. However, the immune response induced by T. spiralis is so variable that this modulation could be of limited value to manage clinical cases of influenza. Nevertheless, the concept that parasites can modulate influenza-induced pathology presents an interesting and potentially useful approach to therapeutics. The local perturbations induced by T. spiralis migration, coincident with the site of influenza infection, certainly warrant further studies.     

Does the redox status of cytochrome C act as a fail-safe mechanism in the regulation of programmed cell death?

It has now become recognized that one of the key events in the induction of apoptosis, or programmed cell death, in both plants and animals is the release of cytochrome c from mitochondria. It is also known that oxidative stress imposed on cells can have a profound effect on the onset or progression of apoptosis. Here, we discuss how the redox status of cytochrome c, and thus its structure, can be altered by the presence of reactive oxygen species (ROS) and reduced glutathione (GSH). We suggest that cytochrome c will only induce programmed cell death if present in the cytoplasm in the oxidized state, and that the presence of high levels of cytoplasmic GSH maintain cytochrome c in an inactive (reduced) state, thus behaving as a fail-safe mechanism if cytochrome c is released by mitochondria when programmed cell death is not the required outcome. If the redox status of the cell is disturbed however, perhaps in the presence of hydrogen peroxide, GSH concentrations will drop, the cellular E(h) will rise, and cytochrome c will tend towards the oxidized state, allowing programmed cell death to proceed. Therefore, we propose that the redox state of cytoplasmic cytochrome c may be a key regulator of programmed cell death.     

PLCζ and its role as a trigger of development in vertebrates

A major unresolved issue in developmental biology is the precise mechanism whereby the sperm activates the oocyte. With the discovery that calcium signals are the primary trigger for oocyte activation, a key remaining question became the identification of the signaling protein that mediates such calcium signals at fertilization. A major step forward came in 2002 with the discovery of a sperm-specific mammalian phospholipase C called phospholipase C zeta (PLCζ), which had the expected properties of the mammalian oocyte activation factor and was subsequently identified in other vertebrate groups. Most recently, defects in PLCζ have been shown to be linked to certain types of male infertility in humans. Despite these advances, many questions remain about the precise mechanism of action of PLCζ and the extent of its role during oocyte activation in the vertebrate kingdom. In this review, we will look at the current state of understanding of PLCζ's mechanism of action and physiological role in mammals and other vertebrates, and identify areas of uncertainty that still remain to be resolved.     

Is the global conservation status assessment of a threatened taxon a utopia?

The signatory countries of the Convention on Biological Diversity agreed to significantly reduce the rate of biodiversity loss by 2010. How will we know, however, if we have achieved this goal? Eight groups of hindrances in evaluating the global conservation status of threatened taxon are identified: (1) the extreme heterogeneity and (2) restricted availability of relevant data; (3) the uncertainty in species number and taxonomic division of the given taxon (Linnean shortfall); (4) the fragmentary distribution knowledge (Wallacean shortfall); (5) the incomplete or incorrect red-listing across the whole distribution area; (6) the lack of homogeneous and exhaustive population trend data; (7) the threat knowledge shortfall; (8) the incomplete general biological knowledge on a given taxon. The Linnean and Wallacean shortfalls lay the foundation of all other hindrances. So long as this dramatic shortfall situation does not change, the adequate assessment of the global status for overwhelming majority of extant taxa will remain a utopia.     

Introduction: why do we need a science of well-being?

Introduction: why do we need a science of well-being?     

Why do birds sleep with one eye open? Light exposure of the chick embryo as a determinant of monocular sleep.

Together with some aquatic mammals, birds exhibit a unique behavioral and electrophysiological state called "unihemispheric sleep," in which one cerebral hemisphere is awake and the other is sleeping. Slow-wave sleep in one hemisphere is associated with closure of the contralateral eye, while the eye contralateral to the awake hemisphere is open; closure of both eyes, in contrast, is associated with bihemispheric slow-wave sleep or with REM sleep. During the last few days of incubation, the chick's embryo is turned in the egg so that it occludes its left eye, whereas light entering through the shell can stimulate the right eye. Here we show that in the first two days after hatching, chicks coming from eggs incubated in the light prevalently slept with their right eye open, whereas those coming from eggs incubated in the dark prevalently slept with their left eye open. Thus, asymmetric light stimulation in the embryo can modulate the left-right direction of eye opening during post-hatching monocular sleep.