The emergence of neural activity and its role in the development of the enteric nervous system

The enteric nervous system (ENS) is a vital part of the autonomic nervous system that regulates many gastrointestinal functions, including motility and secretion. All neurons and glia of the ENS arise from neural crest-derived cells that migrate into the gastrointestinal tract during embryonic development. It has been known for many years that a subpopulation of the enteric neural crest-derived cells expresses pan-neuronal markers at early stages of ENS development. Recent studies have demonstrated that some enteric neurons exhibit electrical activity from as early as E11.5 in the mouse, with further maturation of activity during embryonic and postnatal development. This article discusses the maturation of electrophysiological and morphological properties of enteric neurons, the formation of synapses and synaptic activity, and the influence of neural activity on ENS development.     

Caspase‐7 participates in differentiation of cells forming dental hard tissues

Apoptosis during tooth development appears dependent on the apoptotic executioner caspase‐3, but not caspase‐7. Instead, activated caspase‐7 has been found in differentiated odontoblasts and ameloblasts, where it does not correlate with apoptosis. To further investigate these findings, the mouse incisor was used as a model. Analysis of caspase‐7‐deficient mice revealed a significant thinner layer of hard tissue in the adult incisor. Micro computed tomography scan confirmed this decrease in mineralized tissues. These data strongly suggest that caspase‐7 might be directly involved in functional cell differentiation and regulation of the mineralization of dental matrices.     

Fructose 2, 6-Bisphosphate and Circadian Rhythmicity

We were able to demonstrate the presence of F 2,6-BP in Acetabularia in 7 out of 7 experiments. The amount varies between 4 and 38 pmole par mg protein. We were not able to evidence a circadian rhythm (CR) in its content. However, important fluctuations occur.(Fig. 1). This, of course excludes any precise conclusion about absolute amounts. Biologically active substances often exert an action modulated by circadian time. Thus, the effect of exogenous F 2,6-BP was assayed by fragmenting the long cell in F 2,6-BP-containing sea-water, and then follow growth and cap formation (we performed the experiment at different times during the 24 h cycle, in LD 12:12 conditions. Interestingly, the growth curves (obtained with 4 different concentrations) are statistically accelerated when the treatment had been performed at the beginning of the 24 h cycle (circadian time, CT, 0 is the transition time dark/light), less at CT 9.5, nul at CT 12 and again significant at CT 20. (Fig.IV). There is apparently no strictly defined light effect that could immediately modify the F-2,6-BP level, but there is presumably an important influence of CT-dependent physiological state of the alga. Again, it should be underlined that experimental biology should take time into account.     

The Detection of Novelty Relies on Dopaminergic Signaling: Evidence from Apomorphine's Impact on the Novelty N2

Despite much research, it remains unclear if dopamine is directly involved in novelty detection or plays a role in orchestrating the subsequent cognitive response. This ambiguity stems in part from a reliance on experimental designs where novelty is manipulated and dopaminergic activity is subsequently observed. Here we adopt the alternative approach: we manipulate dopamine activity using apomorphine (D1/D2 agonist) and measure the change in neurological indices of novelty processing. In separate drug and placebo sessions, participants completed a von Restorff task. Apomorphine speeded and potentiated the novelty-elicited N2, an Event-Related Potential (ERP) component thought to index early aspects of novelty detection, and caused novel-font words to be better recalled. Apomorphine also decreased the amplitude of the novelty-P3a. An increase in D1/D2 receptor activation thus appears to potentiate neural sensitivity to novel stimuli, causing this content to be better encoded.     

Evaluating ecosystem effects of climate change on tropical island streams using high spatial and temporal resolution sampling regimes

Climate change is expected to alter precipitation patterns worldwide, which will affect streamflow in riverine ecosystems. It is vital to understand the impacts of projected flow variations, especially in tropical regions where the effects of climate change are expected to be one of the earliest to emerge. Space‐for‐time substitutions have been successful at predicting effects of climate change in terrestrial systems by using a spatial gradient to mimic the projected temporal change. However, concerns have been raised that the spatial variability in these models might not reflect the temporal variability. We utilized a well‐constrained rainfall gradient on Hawaii Island to determine (a) how predicted decreases in flow and increases in flow variability affect stream food resources and consumers and (b) if using a high temporal (monthly, four streams) or a high spatial (annual, eight streams) resolution sampling scheme would alter the results of a space‐for‐time substitution. Declines in benthic and suspended resource quantity (10‐ to 40‐fold) and quality (shift from macrophyte to leaf litter dominated) contributed to 35‐fold decreases in macroinvertebrate biomass with predicted changes in the magnitude and variability in the flow. Invertebrate composition switched from caddisflies and damselflies to taxa with faster turnover rates (mosquitoes, copepods). Changes in resource and consumer composition patterns were stronger with high temporal resolution sampling. However, trends and ranges of results did not differ between the two sampling regimes, indicating that a suitable, well‐constrained spatial gradient is an appropriate tool for examining temporal change. Our study is the first to investigate resource to community wide effects of climate change on tropical streams on a spatial and temporal scale. We determined that predicted flow alterations would decrease stream resource and consumer quantity and quality, which can alter stream function, as well as biomass and habitat for freshwater, marine, and terrestrial consumers dependent on these resources.     

Drosophila biology in the genomic age

Over the course of the past century, flies in the family Drosophilidae have been important models for understanding genetic, developmental, cellular, ecological, and evolutionary processes. Full genome sequences from a total of 12 species promise to extend this work by facilitating comparative studies of gene expression, of molecules such as proteins, of developmental mechanisms, and of ecological adaptation. Here we review basic biological and ecological information of the species whose genomes have recently been completely sequenced in the context of current research.     

The ligand Jelly Belly (Jeb) activates the Drosophila Alk RTK to drive PC12 cell differentiation, but is unable to activate the mouse ALK RTK

The Drosophila Alk receptor tyrosine kinase (RTK) drives founder cell specification in the developing visceral mesoderm and is crucial for the formation of the fly gut. Activation of Alk occurs in response to the secreted ligand Jelly Belly. No homologues of Jelly Belly are described in vertebrates, therefore we have approached the question of the evolutionary conservation of the Jeb-Alk interaction by asking whether vertebrate ALK is able to function in Drosophila. Here we show that the mouse ALK RTK is unable to rescue a Drosophila Alk mutant, indicating that mouse ALK is unable to recognise and respond to the Drosophila Jeb molecule. Furthermore, the overexpression of a dominant-negative Drosophila Alk transgene is able to block the visceral muscle fusion event, which an identically designed dominant-negative construct for the mouse ALK is not. Using PC12 cells as a model for neurite outgrowth, we show here for the first time that activation of dAlk by Jeb results in neurite extension. However, the mouse Alk receptor is unable to respond in any way to the Drosophila Jeb protein in the PC12 system. In conclusion, we find that the mammalian ALK receptor is unable to respond to the Jeb ligand in vivo or in vitro. These results suggest that either (i) mouse ALK and "mouse Jeb" have co-evolved to the extent that mALK can no longer recognise the Drosophila Jeb ligand or (ii) that the mALK RTK has evolved such that it is no longer activated by a Jeb-like molecule in vertebrates.