The Course of Habituation of the Proboscis Extension Reflex Can Be Predicted by Sucrose Responsiveness in Drosophila

The proboscis extension reflex (PER) is triggered when insects’ gustatory receptors contact appetitive stimuli, so it provides a behavioral readout for perceptual encoding of tastants. Research on the experience dependent modulation of PER in Drosophila has been hindered by the difficulty of obtaining reliable measures of memory-driven change in PER probability in the background of larger changes induced by physiological state. In this study, we showed that the course of PER habituation can be predicted by the degree of sucrose responsiveness in Drosophila. We assessed early response parameters, including the number of proboscis extensions and labellar movements in the first five trials, the trial to start responding, and the trial to make the first stop to quantify responsiveness, which predicted the upcoming pattern of both the short-term and 1 hour memory of PER habituation for individual flies. The cAMP signaling pathway mutant rutabaga displayed deficits in attunement of perceptual salience of sucrose to physiological demands and stimulus-driven sensitization

FOXO Regulates Organ-Specific Phenotypic Plasticity In Drosophila

Phenotypic plasticity, the ability for a single genotype to generate different phenotypes in response to environmental conditions, is biologically ubiquitous, and yet almost nothing is known of the developmental mechanisms that regulate the extent of a plastic response. In particular, it is unclear why some traits or individuals are highly sensitive to an environmental variable while other traits or individuals are less so. Here we elucidate the developmental mechanisms that regulate the expression of a particularly important form of phenotypic plasticity: the effect of developmental nutrition on organ size. In all animals, developmental nutrition is signaled to growing organs via the insulin-signaling pathway. Drosophila organs differ in their size response to developmental nutrition and this reflects differences in organ-specific insulin-sensitivity. We show that this variation in insulin-sensitivity is regulated at the level of the forkhead transcription factor FOXO, a negative growth regulator that is activated when nutrition and insulin signaling are low. Individual organs appear to attenuate growth suppression in response to low nutrition through an organ-specific reduction in FOXO expression, thereby reducing their nutritional plasticity. We show that FOXO expression is necessary to maintain organ-specific differences in nutritional-plasticity and insulin-sensitivity, while organ-autonomous changes in FOXO expression are sufficient to autonomously alter an organ's nutritional-plasticity and insulin-sensitivity. These data identify a gene (FOXO) that modulates a plastic response through variation in its expression. FOXO is recognized as a key player in the response of size, immunity, and longevity to changes in developmental nutrition, stress, and oxygen levels. FOXO may therefore act as a more general regulator of plasticity. These data indicate that the extent of phenotypic plasticity may be modified by changes in the expression of genes involved in signaling environmental information to developmental processes

Defining the Boundaries of Development wih Plasticity

International audienceThe concept of plasticity has always been present in the history of developmental biology, both within the theory of epigenesis and within morphogenesis studies. However this tradition relies also upon a genetic conception of plasticity. Founded upon the concepts of "phenotypic plasticity" and "reaction norm," this genetic conception focuses on the array of possible phenotypic change in relation to diversified environments. Another concept of plasticity can be found in recent publications by some developmental biologists (Gilbert, West-Eberhard). I argue that these authors adopt a "broad conception of plasticity" that is closely related to a notion of development as something that is ongoing throughout an organism's lifecycle, and has no clear-cut boundaries. However, I suggest that given a narrow conception of plasticity, one can define temporal boundaries for development that are linked to specific features of the morphological process, which are different from behavioral and physiological processes

Protein Phosphatase 2A Interacts with the Na+,K+-ATPase and Modulates Its Trafficking by Inhibition of Its Association with Arrestin

Background: The P-type ATPase family constitutes a collection of ion pumps that form phosphorylated intermediates during ion transport. One of the best known members of this family is the Na +,K +-ATPase. The catalytic subunit of the Na +,K +-ATPase includes several functional domains that determine its enzymatic and trafficking properties. Methodology/Principal Findings: Using the yeast two-hybrid system we found that protein phosphatase 2A (PP2A) catalytic C-subunit is a specific Na +,K +-ATPase interacting protein. PP-2A C-subunit interacted with the Na +,K +-ATPase, but not with the homologous sequences of the H +,K +-ATPase. We confirmed that the Na +,K +-ATPase interacts with a complex of A- and C-subunits in native rat kidney. Arrestins and G-protein coupled receptor kinases (GRKs) are important regulators of G-protein coupled receptor (GPCR) signaling, and they also regulate Na +,K +-ATPase trafficking through direct association. PP2A inhibits association between the Na +,K +-ATPase and arrestin, and diminishes the effect of arrestin on Na +,K +-ATPase trafficking. GRK phosphorylates the Na +,K +-ATPase and PP2A can at least partially reverse this phosphorylation. Conclusions/Significance: Taken together, these data demonstrate that the sodium pump belongs to a growing list of io

Evolution of sex-specific pace-of-life syndromes: genetic architecture and physiological mechanisms

Sex differences in life history, physiology, and behavior are nearly ubiquitous across taxa, owing to sex-specific selection that arises from different reproductive strategies of the sexes. The pace-of-life syndrome (POLS) hypothesis predicts that most variation in such traits among individuals, populations, and species falls along a slow-fast pace-of-life continuum. As a result of their different reproductive roles and environment, the sexes also commonly differ in pace-of-life, with important consequences for the evolution of POLS. Here, we outline mechanisms for how males and females can evolve differences in POLS traits and in how such traits can covary differently despite constraints resulting from a shared genome. We review the current knowledge of the genetic basis of POLS traits and suggest candidate genes and pathways for future studies. Pleiotropic effects may govern many of the genetic correlations, but little is still known about the mechanisms involved in trade-offs between current and future reproduction and their integration with behavioral variation. We highlight the importance of metabolic and hormonal pathways in mediating sex differences in POLS traits; however, there is still a shortage of studies that test for sex specificity in molecular effects and their evolutionary causes. Considering whether and how sexual dimorphism evolves in POLS traits provides a more holistic framework to understand how behavioral variation is integrated with life histories and physiology, and we call for studies that focus on examining the sex-specific genetic architecture of this integration

Engineering Sciences Supporting Regenerative BioMedicine: Recent Accom-­ plishments

International audienceWe here report recent developments where engineering sciences and mechanics, the basis for reliable design, construction, and maintenance in civil and mechanical engineer-­ ing, have been successfully adapted and trans-­ ferred to the needs of regenerative biomedicine. Thereby, our key target is fracture safety of bony organs and scaffold-­organ compounds.The basis for our safety assessment is a mathematical model for the multiscale ("nano-to-macro") mechanics of bone tissues across the entire vertebrate anial kingdom. This model traces the fracture of bone tissues, donw to sliding phenomena between nanocrystals, and nreaking molecules [4].Besides from setting new standards also in the field of theoretical mechanics itself [7] these mathematical developments, always accompanied by cutting edge experimental activities [6], have paved the way towards computer-aided design of bonestissue engineering systems, as exemplified through a clinically approved hydroxyapatite granule system for dental tissue engineering [9-10]. Such novel methods can also be straightforwardly coupled to valuable information from Computed Tomography: By means of appropriate merging of continuun micromechanics and X-Ray physics, the compositional and mechanical characteristics of the matter found within each and every voxel can be revealved. In this context, we recently deciphered the role of bone anisotropy in assessing biting deformations [5], the resorption properties of TCP biomaterial scaffolds [3], the load carrying behaviorof glass-ceramic scaffolds [8], the safety factor of human vertebrae, and of the aforementioned hydroxyapatite globules under physiological loading [1-2]

Interfacial micromechanics assessment of rheological chain models and their application to early-age creep of concrete

Nanoindentation testing suggests that creep of hydration products is the microscopic reason for macroscopic creep of cementitious materials. This is supported by a multiscale creep model which explains aging creep of young concretes as the consequence of universal creep of hydration products (Scheiner and Hellmich, 2009), whereby the latter is described with a rheological model consisting of linear springs and dashpots. We here extend the investigation of the origin of creep of cementitious materials further down to the nanoscale of hydration products, where we envision solid matter sliding (upon loading) along interfaces which are filled with lubricating thin layers of adsorbed water, i.e. water in a "glassy", "liquid crystal" state. As for the viscous behavior of the interfaces, we follow (Shahidi et al., 2014) and consider that the shear traction acting on an adsorbed water layer is proportional to the shear dislocation rate of the interface, with an interface viscosity as the proportionality constant. Our analysis starts from corresponding anisotropic creep and relaxation tensors of matrix-interface composites containing parallel interfaces (Shahidi et al., 2014). Considering that hydration products contain interfaces oriented isotropically in all space directions, we here compute complete spatial averages of parallel interface-related anisotropic creep and relaxation tensors, in order to derive isotropic creep and relaxation tensor bounds. Comparing them with creep and relaxation functions of the aforementioned rheological model for universal creep of hydration products allows for identification (i) of the interface density and (ii) of the product of interface size and viscosity. Based on the Reusstype creep tensor bound, we obtain, interesting quantitative insight into microstructural features of hydration products