Transformation chez la Drosophile : outils pour l'etude de l'expression et de la regulation des genes

CNRS T 56076 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueSIGLEFRFranc

Deterministic coherence resonance in chaotic lasers with time-delay

TOM 6 813 (poster)A laser with optical feedback may exhibit chaotic dynamics with fast pulses at the timescale of the time delay and much slower power drops. The time between power drops shows however an optimal regularity for a given value of the feedback strength. This resonance has the signature of coherence resonance although it is not driven by noise

Control of basal autophagy rate by vacuolar peduncle

International audienceBasal autophagy is as a compressive catabolic mechanism engaged in the breakdown of damaged macromolecules and organelles leading to the recycling of elementary nutrients. Thought essential to cellular refreshing, little is known about the origin of a constitutional rate of basal autophagy. Here, we found that loss of Drosophila vacuolar peduncle (vap), a presumed GAP enzyme, is associated with enhanced basal autophagy rate and physiological alterations resulting in a wasteful cell energy balance, a hallmark of overactive autophagy. By contrast, starvation-induced autophagy was disrupted in vap mutant conditions, leading to a block of maturation into autolysosomes. This phenotype stem for exacerbated biogenesis of PI(3)P-dependent endomembranes, including autophagosome membranes and ectopic fusions of vesicles. These findings shed new light on the neurodegenerative phenotype found associated to mutant vap adult brains in a former study. A partner of Vap, Sprint (Spri), acting as an endocytic GEF for Rab5, had the converse effect of leading to a reduction in PI(3)P-dependent endomembrane formation in mutants. Spri was conditional to normal basal autophagy and instrumental to the starvation-sensitivity phenotype specific of vap. Rab5 activity itself was essential for PI(3)P and for pre-autophagosome structures formation. We propose that Vap/Spri complexes promote a cell surface-derived flow of endocytic Rab5-containing vesicles, the traffic of which is crucial for the implementation of a basal autophagy rate

Starvation-sensitivity assays define the range of autophagy defects in <i>vap</i> flies.

<p>The survival rate of 3 day-old adult males of indicated genotypes was recorded at 25°C in condition of complete food deprivation (see <b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0209759#pone.0209759.s004" target="_blank">S4A–S4C Fig</a></b> for initial characterization). (A) The <i>vap</i>-dependent starvation sensitivity (white arrow) was compared to weak (<i>Atg8a</i>^<i>1</i>) and strong (<i>Agt8a</i>^<i>2</i>) alleles of <i>Atg8</i>a. <i>Atg8a</i>² flies showed slightly altered development that might contribute to its greater sensitivity to starvation. (B-B’) Starvation sensitivity effect, as assayed at 25°C, is partially recapitulated by flies that were ectopically expressing an <i>UAS-myc</i>:<i>Atg1</i> transgene (Materials and Methods) along fat cell development performed at 25°C (white arrow in B) when driven by <i>cg-Gal4</i>. As a control, there is no detectable starvation sensitivity (as assayed at 25°C) using identical flies (<i>UAS-myc</i>:<i>Atg1</i> /<i>cg-Gal4</i>) that developed at 18°C to minimized transgene expression (white arrow in B’). Ectopic expression of <i>Atg1</i> during development is therefore responsible for the sensitivity effect found in B. (C) The <i>vap</i>-dependent starvation sensitivity is suppressed (white arrow) by co-expressed <i>Atg5(RI)</i> using the broadly expressed <i>arm-Gal4</i> driver. Genotypes. (A) Control: <i>w</i>^<i>1118</i><i>/Y</i>. Assay <i>vap</i>^<i>1</i><i>/Y</i>. <i>Atg8a</i>^<i>1</i><i>/Y</i>. <i>Atg8a</i>^<i>2</i><i>/Y</i>. (B, B’) Control: <i>UAS-myc</i>:<i>Atg1/+</i> and <i>vap</i>^<i>1</i><i>/Y</i> and <i>vap</i>^<i>1</i><i>/Y; cg-GAL4/+</i>. Assay: <i>vap</i>^<i>1</i><i>/Y</i>. <i>cg-GAL4/ UAS-myc</i>:<i>Atg1(RI)/+</i>. (C) Control: <i>arm-GAL4/+</i> and <i>vap</i>^<i>1</i><i>/Y; arm-GAL4/+</i> and <i>arm-GAL4/ UAS-Atg5(RI)/+</i>. Assay: <i>vap</i>^<i>1</i><i>/Y; arm-GAL4/ UAS-Atg5(RI)/+</i>.</p

Changes in the chromatin structure of Drosophila glue genes accompany developmental cessation of transcription in wild type and transformed strains

International audienceThree Drosophila salivary gland glue genes show a dramatic transition in their DNAse I hypersensitive sites during the short period between the late third instar and the white prepupa, which correlates with the cessation of their transcription. In culture cells, where the genes are inactive, there is a chromatin configuration similar to that of prepupal salivary glands. In two transformed fly strains where the sgs3 gene is active at new chromosomal sites, including one in which 2.6 kb of sgs3 upstream sequences have been inverted, the same DNAase I hypersensitive sites and developmental transitions are seen over the same DNA regions. These results, together with the analysis of transformants carrying rearranged sgs3 genes, suggest that there is at least one distal DNAase I hypersensitive site associated with an element of regulation which may be exchanged between sgs genes

Drosophila ALS regulates growth and metabolism through functional interaction with insulin-like peptides.

In metazoans, factors of the insulin family control growth, metabolism, longevity, and fertility in response to environmental cues. In Drosophila, a family of seven insulin-like peptides, called Dilps, activate a common insulin receptor. Some Dilp peptides carry both metabolic and growth functions, raising the possibility that various binding partners specify their functions. Here we identify dALS, the fly ortholog of the vertebrate insulin-like growth factor (IGF)-binding protein acid-labile subunit (ALS), as a Dilp partner that forms a circulating trimeric complex with one molecule of Dilp and one molecule of Imp-L2, an IgG-family molecule distantly related to mammalian IGF-binding proteins (IGFBPs). We further show that dALS antagonizes Dilp function to control animal growth as well as carbohydrate and fat metabolism. These results lead us to propose an evolutionary perspective in which ALS function appeared prior to the separation between metabolic and growth effects that are associated with vertebrate insulin and IGFs