Unconventional bed mates: Gaia and the selfish gene

In this forum, David M. Wilkinson argued that Gaia-type phenomena can be explained by conventional ecological ideas meaning that such phenomena do not require major changes to existing ecological or evolutionary theory. Overstating my case a little, I will argue that a reconciliation between Gaia and Darwinism will not be conventional in the sense of mainstream ecology. The main addition of this essay is an exploration in how far the claim that the atmosphere is an extension of life on Earth is logically correct. In a thought experiment, the idea of extended phenotypes by Richard Dawkins can be integrated with the one of Gaia. The problem of cheats remains pertinent, however, because the atmosphere will not select differentially between cheats and non-cheats. Conclusion: Gaia-type phenomena will be by-products of naturally selected traits. As such they are not jeopardised by cheats, because side effects can be free to self-organise, while the main effects will be naturally selected for evolutionarily stable states. Understanding the laws of self-organisation of such side effects will be of major importance to all environmental sciences.     

Haemorrhagic cytology samples – how to get the best diagnostic results

OBJECTIVE: To describe and evaluate the value of a simple filtration technique for use in processing haemorrhagic samples for cytomorphological evaluation and immunocytochemistry. METHODS: One hundred and sixty haemorrhagic cytological samples (133 FNAs, 27 effusions) received in our laboratory from August 2002 to September 2005 were included in this study. After preparing two smears for diagnostic evaluation, the residual sample was suspended in 2 ml of a cell medium prepared in our laboratory. These primary haemorrhagic suspensions were filtered through disposable nylon filter devices and the cells deposited on the upper membrane surface were transferred into 2 ml of fresh cell medium. From all three fractions - primary cell suspension, filter deposit and filtrate - cytospins were prepared and stained by Giemsa or Papanicolaou methods. Cytospins were examined under the microscope for the presence of diagnostic cells, red blood cells (RBCs) and debris. Additional cytospins for immunocytochemistry were prepared at the cytopathologist's request. RESULTS: RBCs and debris were successfully removed in 142 out of 160 haemorrhagic samples (88%) by using this new filtration technique. In all these cases the tumour cells were well presented and allowed substantially improved cytomorphological evaluation. Immunocytochemical staining was performed on 112 filtered samples with three different markers per case on average. Filtration did not improve the quality of cytospins in 18/160 haemorrhagic samples, mostly attributable to insufficient numbers of diagnostic cells in the original samples. CONCLUSION: The presented filtration technique is very simple and quick. It substantially improves the quality of haemorrhagic samples for cytomorphological evaluation; moreover, the samples are well suited for multiple immunocytochemical stainings.     

Getting out alive: how predators affect the decision to metamorphose

Metamorphosis has intrigued biologists for a long time as an extreme form of complex life cycles that are ubiquitous in animals. While investigated from a variety of perspectives, the ecological focus has been on identifying and understanding the ecological factors that affect an individual’s decision on when, and at what size, to metamorphose. Predation is a major factor that affects metamorphic decisions and a recent review by Benard (Annu Rev Ecol Evol Syst 35:651–673, 2004)) documented how predator cues induce metamorphic changes relative to model predictions. Importantly, however, real predators affect larval prey via several mechanisms beyond simple induction. In this paper, I contrast the leading models of metamorphosis, provide an overview of the multiple ways that predators can directly and indirectly affect larval growth and development (via induction, thinning, and selection), and identify how each process should affect the time to and size at metamorphosis. With this mechanistic foundation established, I then turn to the well-studied model system of larval amphibians to synthesize studies on: (1) caged predators (which cause only induction), and (2) lethal predators (which cause induction, thinning, and selection). Among the caged-predator studies, the chemical cues emitted by predators rarely induce a smaller size at metamorphosis or a shorter time to metamorphosis, which is in direct contrast to theoretical predictions but in agreement with Benard’s (Annu Rev Ecol Evol Syst 35:651–673, 2004) review based on a considerably smaller dataset. Among the lethal-predator studies, there is a diversity of outcomes depending upon the relative importance of induction versus thinning with the relative importance of the two processes appearing to change with larval density. Finally, I review the persistent effects of larval predators after metamorphosis including both phenotypic and fitness effects. At the end, I outline a number of future directions to allow researchers to continue gaining insight into how predators affect the metamorphic decisions of their prey. Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Xenopus connexins: how frogs bridge the gap

Animal species use specialized cell-to-cell channels, called gap junctions, to allow for a direct exchange of ions and small metabolites between their cells' cytoplasm. In invertebrates, gap junctions are formed by innexins, while vertebrates use connexin (Cx) proteins as gap-junction-building blocks. Recently, innexin homologs have been found in vertebrates and named pannexins. From progress in the different genome projects, it has become evident that every class of vertebrates uses their own unique set of Cxs to build their gap junctions. Here, we review all known Xenopus Cxs with respect to their expression, regulation, and function. We compare Xenopus Cxs with those of zebrafish and mouse, and provide evidence for the existence of several additional, non-identified, amphibian Cxs. Finally, we identify two new Xenopus pannexins by screening EST libraries.     

Source–sink dynamics: how sinks affect demography of sources

Models of source–sink population dynamics have to make assumptions about whether, and eventually how, demographic parameters in source habitats are dependent on the demography in sink habitats. However, the empirical basis for making such assumptions has been weak. Here we report a study on experimental root vole populations, where estimates of demographic parameters were contrasted between source patches in source–sink (treatment) and source–source systems (control). In the presence of a sink patch (simulated by a pulsed removal of immigrants), source‐patch populations failed to increase over the breeding season, mainly due to a high spatially density‐dependent dispersal rate from source to sink patches. The per capita recruitment rate was almost two times higher in source–sink than in the source–source systems, but this did not compensate for the loss rate due to dispersal from source to sink patches. Sex ratio in the source–sink systems became less female biased, probably as a result of an enhanced frequency of dispersal movements in females. Good knowledge of the degree of density‐and habitat‐dependent dispersal is critical for predicting the dynamics of source–sink populations.     

When, where and how the bridge breaks: anaphase bridge breakage plays a crucial role in gene amplification and HSR generation

Amplified genes are frequently localized on extrachromosomal double minutes (DMs) or in chromosomal homogeneously staining regions (HSRs). We previously showed that a plasmid bearing a mammalian replication initiation region could efficiently generate DMs and HSRs after transfection into human tumor cell lines. The Breakage-Fusion-Bridge (BFB) cycle model, a classical model that explains how HSRs form, could also be used to explain how the transfected plasmids generate HSRs. The BFB cycle model involves anaphase bridge formation due to the presence of dicentric chromosomes, followed by the breakage of the bridge. In this study, we used our plasmid-based model system to analyze how anaphase bridges break during mitosis. Dual-color fluorescence in situ hybridization analyses revealed that anaphase bridges were most frequently severed in their middle irrespective of their lengths, which suggests that a structurally fragile site exists in the middle of the anaphase bridge. Breakage of the chromosomal bridges occurred prior to nuclear membrane reformation and the completion of cytokinesis, which indicates that mechanical tension rather than cytokinesis is primarily responsible for severing anaphase bridges. Time-lapse observation of living cells revealed that the bridges rapidly shrink after being severed. If HSR length was extended too far, the bridge could no longer be resolved and became tangled depending on the tension. The unbroken bridge appeared to inhibit the completion of cytokinesis. These observations strongly suggest that anaphase bridges are highly elastic and that the length of the spindle axis determines the maximal HSR length.