Variable-delay feedback control of unstable steady states in retarded time-delayed systems

We study the stability of unstable steady states in scalar retarded time-delayed systems subjected to a variable-delay feedback control. The important aspect of such a control problem is that time-delayed systems are already infinite-dimensional before the delayed feedback control is turned on. When the frequency of the modulation is large compared to the system's dynamics, the analytic approach consists of relating the stability properties of the resulting variable-delay system with those of an analogous distributed delay system. Otherwise, the stability domains are obtained by a numerical integration of the linearized variable-delay system. The analysis shows that the control domains are significantly larger than those in the usual time-delayed feedback control, and that the complexity of the domain structure depends on the form and the frequency of the delay modulation.Comment: 13 pages, 8 figures, RevTeX, accepted for publication in Physical Review

Phase equilibria and phase transformations in the Ti-rich corner of the Fe-Ni-Ti system

While the main features of the Fe-Ni-Ti system are well known at low Ti content, literature review of the Ti-rich corner revealed inconsistencies between experimental reports. This investigation presents new experimental results, defined to remove the uncertainties concerning melting behavior and solid-state phase equilibria of the (Ni,Fe)Ti2 phase with the adjacent (Fe,Ni)Ti (B2, CsCl-type structure) and Beta-Ti (A2, W-type) phases. Six samples have been prepared and examined by differential thermal analysis performed in yttria and alumina crucibles, and by scanning electron microscopy in the as-cast state as well as equilibrated at 900°C

Shar-pei Mediates Cell Proliferation Arrest During Imaginal Disc Growth in Drosophila

During animal development, organ size is determined primarily by the amount of cell proliferation, which must be tightly regulated to ensure the generation of properly proportioned organs. However, little is known about the molecular pathways that direct cells to stop proliferating when an organ has attained its proper size. We have identified mutations in a novel gene, shar-pei, that is required for proper termination of cell proliferation during Drosophila imaginal disc development. Clones of shar-pei mutant cells in imaginal discs produce enlarged tissues containing more cells of normal size. We show that this phenotype is the result of both increased cell proliferation and reduced apoptosis. Hence,shar-pei restricts cell proliferation and promotes apoptosis. By contrast, shar-pei is not required for cell differentiation and pattern formation of adult tissue. Shar-pei is also not required for cell cycle exit during terminal differentiation, indicating that the mechanisms directing cell proliferation arrest during organ growth are distinct from those directing cell cycle exit during terminal differentiation. shar-pei encodes a WW-domain-containing protein that has homologs in worms, mice and humans, suggesting that mechanisms of organ growth control are evolutionarily conserved

Late-Holocene climate dynamics recorded in the peat bogs of Tierra del Fuego, South America

The ombrotrophic peat bogs of Tierra del Fuego are located within the southern westerly wind belt (SWWB), which dominates climate variability in this region. We have reconstructed late-Holocene water-table depths from three peat bogs and aimed to relate these records to shifts in regional climate. Water-table depths were quantified by the analysis of testate amoeba assemblages, and a regional transfer function was used to infer past water-table depths. During the last 2000 years, testate amoeba assemblages have been relatively stable, with a dominance of Difflugia pulex and Difflugia pristis type, and an increase in Assulina muscorum and other Euglyphida at the top of each section. Multivariate analyses show that water-table depth remained the main environmental variable explaining assemblages along the TiA12 core, but reconstructions were not significant for the two other cores. In line with the low variability in assemblages, water tables were relatively stable during the last 2000 years. Slightly wetter conditions were found between ~1400 and 900 cal. BP and a pronounced recent dry shift was reconstructed in all of the three peat profiles. Considering the regional climatic context, this recent shift may have been forced by a decrease in precipitation and warmer conditions linked to an increase in the importance of the SWWB. Nevertheless, we cannot exclude the influence of higher UV-B radiation resulting from the local degradation of the ozone layer since the late 1970s, which may have had an additional effect on the relative presence of A. muscorum in the southern Patagonian region

Eps15 and Dap160 control synaptic vesicle membrane retrieval and synapse development

Epidermal growth factor receptor pathway substrate clone 15 (Eps15) is a protein implicated in endocytosis, endosomal protein sorting, and cytoskeletal organization. Its role is, however, still unclear, because of reasons including limitations of dominant-negative experiments and apparent redundancy with other endocytic proteins. We generated Drosophila eps15-null mutants and show that Eps15 is required for proper synaptic bouton development and normal levels of synaptic vesicle (SV) endocytosis. Consistent with a role in SV endocytosis, Eps15 moves from the center of synaptic boutons to the periphery in response to synaptic activity. The endocytic protein, Dap160/intersectin, is a major binding partner of Eps15, and eps15 mutants phenotypically resemble dap160 mutants. Analyses of eps15 dap160 double mutants suggest that Eps15 functions in concert with Dap160 during SV endocytosis. Based on these data, we hypothesize that Eps15 and Dap160 promote the efficiency of endocytosis from the plasma membrane by maintaining high concentrations of multiple endocytic proteins, including dynamin, at synapses

A Screen for Genes Expressed in the Olfactory Organs of Drosophila melanogaster Identifies Genes Involved in Olfactory Behaviour

BACKGROUND: For insects the sense of smell and associated olfactory-driven behaviours are essential for survival. Insects detect odorants with families of olfactory receptor proteins that are very different to those of mammals, and there are likely to be other unique genes and genetic pathways involved in the function and development of the insect olfactory system. METHODOLOGY/PRINCIPAL FINDINGS: We have performed a genetic screen of a set of 505 Drosophila melanogaster gene trap insertion lines to identify novel genes expressed in the adult olfactory organs. We identified 16 lines with expression in the olfactory organs, many of which exhibited expression of the trapped genes in olfactory receptor neurons. Phenotypic analysis showed that six of the lines have decreased olfactory responses in a behavioural assay, and for one of these we showed that precise excision of the P element reverts the phenotype to wild type, confirming a role for the trapped gene in olfaction. To confirm the identity of the genes trapped in the lines we performed molecular analysis of some of the insertion sites. While for many lines the reported insertion sites were correct, we also demonstrated that for a number of lines the reported location of the element was incorrect, and in three lines there were in fact two pGT element insertions. CONCLUSIONS/SIGNIFICANCE: We identified 16 new genes expressed in the Drosophila olfactory organs, the majority in neurons, and for several of the gene trap lines demonstrated a defect in olfactory-driven behaviour. Further characterisation of these genes and their roles in olfactory system function and development will increase our understanding of how the insect olfactory system has evolved to perform the same essential function to that of mammals, but using very different molecular genetic mechanisms

Activity-Independent Prespecification of Synaptic Partners in the Visual Map of Drosophila

SummarySpecifying synaptic partners and regulating synaptic numbers are at least partly activity-dependent processes during visual map formation in all systems investigated to date [1–5]. In Drosophila, six photoreceptors that view the same point in visual space have to be sorted into synaptic modules called cartridges in order to form a visuotopically correct map [6, 7]. Synapse numbers per photoreceptor terminal and cartridge are both precisely regulated [8–10]. However, it is unknown whether an activity-dependent mechanism or a genetically encoded developmental program regulates synapse numbers. We performed a large-scale quantitative ultrastructural analysis of photoreceptor synapses in mutants affecting the generation of electrical potentials (norpA, trp;trpl), neurotransmitter release (hdc, syt), vesicle endocytosis (synj), the trafficking of specific guidance molecules during photoreceptor targeting (sec15), a specific guidance receptor required for visual map formation (Dlar), and 57 other novel synaptic mutants affecting 43 genes. Remarkably, in all these mutants, individual photoreceptors form the correct number of synapses per presynaptic terminal independently of cartridge composition. Hence, our data show that each photoreceptor forms a precise and constant number of afferent synapses independently of neuronal activity and partner accuracy. Our data suggest cell-autonomous control of synapse numbers as part of a developmental program of activity-independent steps that lead to a “hard-wired” visual map in the fly brain

The Nicotinic Acetylcholine Receptor Dα7 Is Required for an Escape Behavior inDrosophila

Acetylcholine is the major excitatory neurotransmitter in the central nervous system of insects. Mutant analysis of the Dα7 nicotinic acetylcholine receptor (nAChR) ofDrosophila shows that it is required for the giant fiber-mediated escape behavior. The Dα7 protein is enriched in the dendrites of the giant fiber, and electrophysiological analysis of the giant fiber circuit showed that sensory input to the giant fiber is disrupted, as is transmission at an identified cholinergic synapse between the peripherally synapsing interneuron and the dorsal lateral muscle motor neuron. Moreover, we found thatgfA(1), a mutation identified in a screen for giant fiber defects more than twenty years ago, is an allele ofDα7. Therefore, a combination of behavioral, electrophysiological, anatomical, and genetic data indicate an essential role for the Dα7 nAChR in giant fiber-mediated escape inDrosophila

Reduced body weight is a common effect of gene knockout in mice

<p>Abstract</p> <p>Background</p> <p>During a search for obesity candidate genes in a small region of the mouse genome, we noticed that many genes when knocked out influence body weight. To determine whether this was a general feature of gene knockout or a chance occurrence, we surveyed the Jackson Laboratory Mouse Genome Database for knockout mouse strains and their phenotypes. Body weights were not available for all strains so we also obtained body weight information by contacting a random sample of investigators responsible for a knockout strain.</p> <p>Results</p> <p>We classified each knockout mouse strain as (1) lighter and smaller, (2) larger and heavier, or (3) the same weight, relative to control mice. We excluded knockout strains that died early in life, even though this type of lethality is often associated with a small embryo or reduced body size. Based on a dataset of 1,977 knockout strains, we found that that 31% of viable knockout mouse strains weighed less and an additional 3% weighed more than did controls.</p> <p>Conclusion</p> <p>Body weight is potentially a latent variable in about a third of experiments that use knockout mice and should be considered in interpreting experimental outcomes, e.g., in studies of hypertension, drug and hormone metabolism, organ development, cell proliferation and apoptosis, digestion, heart rate, or atherosclerosis. If we assume that the knockout genes we surveyed are representative then upward of 6,000 genes are predicted to influence the size of a mouse. Body weight is highly heritable, and numerous quantitative trait loci have been mapped in mice, but "multigenic" is an insufficient term for the thousands of loci that could contribute to this complex trait.</p