Towards autonomic networking and selfconfigurating routers

IP Networks, and particularly the Internet, were proposed to be a simple and robust support for heterogeneous communications. This implies that only basic controls have to be done by network elements. Connection management, along with transport, and more generally communication management, has to be done by the terminals. For example, error detection mechanisms, error recovery mechanisms with “Slow Start”, are implemented within the transport protocol, managed by the terminals. However, integration of new services and increasing need for QoS require the network to be more and more flexible and adaptive. New algorithms and protocols are then proposed to address these issues, and include new configuration layers. Manual configuration of such network architectures is then very complex, if not impossible. We think that future core network elements will have to be more adaptive, but also more autonomic. Autoconfiguration is indeed a necessary condition to integrate new services in the network. We believe that autoconfiguration requires new knowledge provisioning and computing policies. This paper then presents an architecture of software agents, collaborative and autonomic. These agents are embedded inside the routers. Their role is to share local and situated knowledge, in order to control and optimize the existing control mechanism of the router.5th IFIP International Conference on Network Control & Engineering for QoS, Security and MobilityRed de Universidades con Carreras en Informática (RedUNCI

The Enigma of Store-Operated Ca2+-Entry in Neurons: Answers from the Drosophila Flight Circuit

In neurons a well-defined source of signaling Ca2+ is the extracellular medium. However, as in all metazoan cells, Ca2+ is also stored in endoplasmic reticular compartments inside neurons. The relevance of these stores in neuronal function has been debatable. The Orai gene encodes a channel that helps refill these stores from the extracellular medium in non-excitable cells through a process called store-operated Ca2+ entry or SOCE. Recent findings have shown that raising the level of Orai or its activator STIM, and consequently SOCE in neurons, can restore flight to varying extents to Drosophila mutants for an intracellular Ca2+-release channel – the inositol 1,4,5-trisphosphate receptor (InsP3R). Both intracellular Ca2+-release and SOCE appear to function in neuro-modulatory domains of the flight circuit during development and acute flight. These findings raise exciting new possibilities for the role of SOCE in vertebrate motor circuit function and the treatment of neurodegenerative disorders where intracellular Ca2+ signaling has been implicated as causative

Patterns of Gene Expression in Drosophila InsP3 Receptor Mutant Larvae Reveal a Role for InsP3 Signaling in Carbohydrate and Energy Metabolism

Background: The Inositol 1,4,5-trisphosphate receptor (InsP3R) is an InsP3 gated intracellular Ca 2+-release channel. Characterization of Drosophila mutants for the InsP3R has demonstrated that InsP3-mediated Ca 2+ release is required in Drosophila larvae for growth and viability. Methodology/Principal Findings: To understand the molecular basis of these growth defects a genome wide microarray analysis has been carried out with larval RNA obtained from a strong InsP3R mutant combination in which 1504 independent genes were differentially regulated with a log 2 of fold change of 1 or more and P,0.05. This was followed by similar transcript analyses from InsP3R mutants where growth defects were either suppressed by introduction of a dominant suppressor or rescued by ectopic expression of an InsP3R transgene in the Drosophila insulin like peptide-2 (Dilp2) producing cells. Conclusions/Significance: These studies show that expression of transcripts related to carbohydrate and amine metabolism is altered in InsP 3 receptor mutant larvae. Moreover, from a comparative analysis of genes that are regulated in the suppressed and rescued conditions with the mutant condition, it appears that the organism could use differen

Altered levels of Gq activity modulate axonal pathfinding in Drosophila

A majority of neurons that form the ventral nerve cord send out long axons that cross the midline through anterior or posterior commissures. A smaller fraction extend longitudinally and never cross the midline. The decision to cross the midline is governed by a balance of attractive and repulsive signals. We have explored the role of a G-protein, Gαq, in altering this balance in Drosophila. A splice variant of Gαq, dgqα3, is expressed in early axonal growth cones, which go to form the commissures in the Drosophila embryonic CNS. Misexpression of a gain-of-function transgene of dgqα3 (AcGq3) leads to ectopic midline crossing. Analysis of the AcGq3 phenotype in roundabout and frazzled mutants shows that AcGq3 function is antagonistic to Robo signaling and requires Frazzled to promote ectopic midline crossing. Our results show for the first time that a heterotrimeric G-protein can affect the balance of attractive versus repulsive cues in the growth cone and that it can function as a component of signaling pathways that regulate axonal pathfinding

Preferential expression of biotransformation enzymes in the olfactory organs of Drosophila melanogaster, the antennae

Biotransformation enzymes have been found in the olfactory epithelium of vertebrates. We now show that in Drosophila melanogaster, a UDP-glycosyltransferase (UGT), as well as a short chain dehydrogenase/reductase and a cytochrome P450 are expressed specifically or preferentially in the olfactory organs, the antennae. The evolutionarily conserved expression of biotransformation enzymes in olfactory organs suggests that they play an important role in olfaction. In addition, we describe five Drosophila UGTs belonging to two families. All five UGTs contain a putative transmembrane domain at their C terminus as is the case for vertebrate UGTs where it is required for enzymatic activity. The primary sequence of the C terminus, including part of the transmembrane domain, differs between the two families but is highly conserved not only within each Drosophila family, but also between the members of one of the Drosophila families and vertebrate UGTs. The partial overlap of the conserved primary sequence with the transmembrane domain suggests that this part of the protein is involved in specific interactions occurring at the membrane surface. The presence of different C termini in the two Drosophilafamilies suggests that they interact with different targets, one of which is conserved between Drosophila and vertebrates

Agent-based self-management of MPLS DiffServ-TE domain

MPLS DiffServ-TE presents the solution awaited so much by the network service providers by allowing a differentiation of services and a traffic engineering based on a fast packet switching technology. However, the management of such a network is not a simple function and could not be done manually. In this paper, we propose a novel architecture based on the Multi-Agent Systems (MAS) capable of managing automatically MPLS DiffServ-TE domains. Based on the network states, our intelligent agents take the appropriate decisions. They, for example, reconfigure the network accordingly5th IFIP International Conference on Network Control & Engineering for QoS, Security and MobilityRed de Universidades con Carreras en Informática (RedUNCI

Complete nucleotide sequence of an unusual mobile element from Trypanosoma brucei

The complete nucleotide sequence of a mobile element from Trypanosoma brucei is presented along with the sequence of its target site, which shows that the insertion has generated a 7 base pair direct repeat. The cloned copy of the element is a dimeric structure, one end of each monomer consisting of a stretch of 14 A residues preceded by a putative trypanosome polyadenylation signal. Six base pairs of DNA of unknown origin are found in the dimer between the two copies of the element. Evidence suggests that the element is present in the genome mainly as a monomer whose sequence is conserved across several species of trypanosome. The element contains an open reading frame encoding the same 160 amino acid protein in both sequenced copies and is extensively transcribed from both strands

IP3 receptors and Ca2+ entry

Inositol 1,4,5-trisphosphate receptors (IP3R) are the most widely expressed intracellular Ca2+ release channels. Their activation by IP3 and Ca2+ allows Ca2+ to pass rapidly from the ER lumen to the cytosol. The resulting increase in cytosolic [Ca2+] may directly regulate cytosolic effectors or fuel Ca2+ uptake by other organelles, while the decrease in ER luminal [Ca2+] stimulates store-operated Ca2+ entry (SOCE). We are close to understanding the structural basis of both IP3R activation, and the interactions between the ER Ca2+-sensor, STIM, and the plasma membrane Ca2+ channel, Orai, that lead to SOCE. IP3Rs are the usual means through which extracellular stimuli, through ER Ca2+ release, stimulate SOCE. Here, we review evidence that the IP3Rs most likely to respond to IP3 are optimally placed to allow regulation of SOCE. We also consider evidence that IP3Rs may regulate SOCE downstream of their ability to deplete ER Ca2+ stores. Finally, we review evidence that IP3Rs in the plasma membrane can also directly mediate Ca2+ entry in some cells

Loss of IP₃ receptor function in neuropeptide secreting neurons leads to obesity in adult Drosophila

Background: Intracellular calcium signaling regulates a variety of cellular and physiological processes. The inositol 1,4,5 trisphosphate receptor (IP3R) is a ligand gated calcium channel present on the membranes of endoplasmic reticular stores. In previous work we have shown that Drosophila mutants for the IP3R (itprku) become unnaturally obese as adults with excessive storage of lipids on a normal diet. While the phenotype manifests in cells of the fat body, genetic studies suggest dysregulation of a neurohormonal axis. Results: We show that knockdown of the IP3R, either in all neurons or in peptidergic neurons alone, mimics known itpr mutant phenotypes. The peptidergic neuron domain includes, but is not restricted to, the medial neurosecretory cells as well as the stomatogastric nervous system. Conversely, expression of an itpr+ cDNA in the same set of peptidergic neurons rescues metabolic defects of itprku mutants. Transcript levels of a gene encoding a gastric lipase CG5932 (magro), which is known to regulate triacylglyceride storage, can be regulated by itpr knockdown and over-expression in peptidergic neurons. Thus, the focus of observed itpr mutant phenotypes of starvation resistance, increased body weight, elevated lipid storage and hyperphagia derive primarily from peptidergic neurons. Conclusions: The present study shows that itpr function in peptidergic neurons is not only necessary but also sufficient for maintaining normal lipid metabolism in Drosophila. Our results suggest that intracellular calcium signaling in peptidergic neurons affects lipid metabolism by both cell autonomous and non-autonomous mechanisms