Hervé Tricoire

ORCID: 0000-0001-9404-5282
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About
Contact & Profiles
Research Areas
  • Genetics, Aging, and Longevity in Model Organisms
  • Genetic Neurodegenerative Diseases
  • Developmental Biology and Gene Regulation
  • Mitochondrial Function and Pathology
  • Genomics and Chromatin Dynamics
  • Nuclear physics research studies
  • Neurobiology and Insect Physiology Research
  • Insect Resistance and Genetics
  • Invertebrate Immune Response Mechanisms
  • Nuclear Physics and Applications
  • Advanced Chemical Physics Studies
  • Wnt/β-catenin signaling in development and cancer
  • Hedgehog Signaling Pathway Studies
  • Insect symbiosis and bacterial influences
  • Cold Atom Physics and Bose-Einstein Condensates
  • Insect Utilization and Effects
  • High-Energy Particle Collisions Research
  • Ubiquitin and proteasome pathways
  • Microfluidic and Capillary Electrophoresis Applications
  • RNA Research and Splicing
  • Sleep and Wakefulness Research
  • Radiation Detection and Scintillator Technologies
  • Cancer-related gene regulation
  • Photocathodes and Microchannel Plates
  • Radiation Therapy and Dosimetry

Centre National de la Recherche Scientifique
1997-2021

Université Paris Cité
2009-2021

Unit of Functional and Adaptive Biology
2009-2021

Délégation Paris 7
2000-2018

Sorbonne Paris Cité
2015-2018

Institut Jacques Monod
1995-2015

Sorbonne Université
1998-2002

Institut de Physique
1985-2001

Institut National de Physique Nucléaire et de Physique des Particules
1997

Université Paris-Saclay
1995-1997

Abstract Background During their life, multicellular organisms are challenged with oxidative stress. It is generated by several reactive oxygen species (ROS), may limit lifespan and has been related to human diseases. ROS can generate a wide variety of defects in many cellular components thus the response organism stress share some features other responses. Conversely, spite recent progress, complete functional analysis transcriptional responses different stresses model still missing. In...

10.1186/1471-2164-5-74 article EN cc-by BMC Genomics 2004-09-30

Abstract Aging’s most obvious characteristic is the time dependent increase of an individual’s probability to die. This lifelong process accompanied by a large number molecular and physiological changes. Although numerous genes involved in aging have been identified past decades its leading factors yet be determined. To identify very processes driving we developed years assay physiologically old individuals synchronized population Drosophila melanogaster . Those show age-dependent intestinal...

10.1038/srep23523 article EN cc-by Scientific Reports 2016-03-22

Glia are important modulators of neural activity, yet few studies link glia to sleep regulation. We find that blocking activity the endocytosis protein, dynamin, in adult Drosophila increases and enhances need, manifest as resistance deprivation. Surface comprising fly equivalent blood-brain barrier (BBB) mediate effect dynamin on sleep. Blocking surface causes ultrastructural changes, albeit without compromising integrity barrier. Supporting a role for endocytic trafficking sleep, screen...

10.7554/elife.43326 article EN cc-by eLife 2018-11-26

Abstract Background During the last two decades progress in genetics of aging invertebrate models such as C. elegans and D. melanogaster has clearly demonstrated existence regulatory pathways that control rate these organisms, insulin-like pathway, Jun kinase pathway Sir2 deacetylase pathway. Moreover, it was rapidly shown some are conserved from yeast to humans. In parallel genetic studies, genomic expression approches have given us significant information on gene modifications occur during...

10.1186/1471-2164-7-69 article EN cc-by BMC Genomics 2006-04-04

Septic injury triggers a rapid and widespread response in Drosophila adults that involves the up‐regulation of many genes required to combat infection for wound healing. Genome‐wide expression profiling has already demonstrated this is controlled by signaling through Toll, Imd, JAK‐STAT JNK pathways. Using oligonucleotide microarrays, we now demonstrate MAPKKK Mekk1 regulates small subset induced septic including Turandot ( Tot ) stress genes. Our analysis indicates show complex regulation...

10.1111/j.1365-2443.2006.00953.x article EN Genes to Cells 2006-02-28

Spinocerebellar ataxia 7 (SCA7) is a neurodegenerative disease caused by polyglutamine (polyQ) expansion in the ataxin (ATXN7) protein, member of multiprotein complex involved histone acetylation. We have created conditional Drosophila model SCA7 which expression truncated ATXN7 (ATXN7T) with pathogenic polyQ induced neurons adult flies. In this model, mutant ATXN7T accumulated neuronal intranuclear inclusions containing ubiquitin, 19S proteasome subunit, and HSP70 (heat shock protein 70),...

10.1523/jneurosci.5453-06.2007 article EN cc-by-nc-sa Journal of Neuroscience 2007-03-07

Cardiac aging is a complex process, which influenced by both environmental and genetic factors. Deciphering the mechanisms involved in heart senescence therefore requires identifying molecular pathways that are affected age controlled conditions. We describe functional genomic investigation of control cardiac Drosophila. Molecular signatures were identified differential transcriptome analysis followed detailed bio-informatic analysis. This approach implicated JNK/dJun pathway transcription...

10.1371/journal.pgen.1003081 article EN cc-by PLoS Genetics 2012-11-29

Abstract fused (fu) is a segment polarity gene that encodes putative serine/threonine kinase. A complete suppressor of the embryonic and adult phenotypes fu mutants, Suppressor (Su(fu)), was previously described. The amorphic Su(fu) mutation viable displays no phenotype by itself. We have used this as tool to perform genetic dissection gene. Analysis interaction between 33 alleles shows they belong three different classes. Defects due class I are fully suppressed Su(fu). Class II lead new in...

10.1093/genetics/135.4.1047 article EN Genetics 1993-12-01

Significance Ataxin-3 is the affected protein in neurodegenerative disorder spinocerebellar ataxia type 3 (SCA3). Nuclear ataxin-3 has been linked to disease progression and formation of aggregates. Our present findings implicate karyopherin alpha (KPNA3) vitro transport SCA3-related phenotypes Drosophila mouse models. We have demonstrated that altering proteins an effect on both pathogenic mechanisms (e.g., intracellular localization aggregates) key features toxicity such as anxiety, total...

10.1073/pnas.1716071115 article EN Proceedings of the National Academy of Sciences 2018-02-23

Abstract Suppressor of fused, Su(fu), was identified as a semi-dominant suppressor the putative serine/threonine kinase encoded by segment polarity gene fused in Drosophila melanogaster. The amorphic Su(fu) mutation is viable, shows maternal effect and displays no phenotype itself. mutations are often found associated to karmoisin (kar) but two complementation groups can be clearly identified. By using differential hybridization screening method, we have cloned region chromosomal...

10.1093/genetics/140.2.587 article EN Genetics 1995-06-01

The circular polarization ${P}_{\ensuremath{\gamma}}$ of deexcitation $\ensuremath{\gamma}$ rays has been measured in coincidence with fast charged particles from reactions induced by light heavy ions at $\frac{E}{A}\ensuremath{\approx}8$ MeV. Polarizations up to $|{P}_{\ensuremath{\gamma}}|\ensuremath{\approx}0.3$ were observed. variations sign and magnitude the particle type, energy, angle, target mass reveal effects particle-target interaction during a tangential passage along nucleus.

10.1103/physrevlett.53.1630 article EN Physical Review Letters 1984-10-22

Aging is commonly described as being a continuous process affecting progressively organisms time passes. This results in progressive decrease individuals fitness through wide range of both organismal–decreased motor activity, fertility, resistance to stress–and molecular phenotypes–decreased protein and energy homeostasis, impairment insulin signaling. In the past 20 years, numerous genes have been identified playing major role aging process, yet little known about events leading that loss...

10.1371/journal.pone.0141920 article EN cc-by PLoS ONE 2015-11-03

Friedreich's ataxia (FRDA), the most common hereditary ataxia, is characterized by progressive degeneration of central and peripheral nervous system, hypertrophic cardiomyopathy a high risk diabetes. FRDA caused abnormally low levels frataxin, highly conserved mitochondrial protein. Drosophila has been previously successfully used to model in various cell types, including neurons glial cells. Here, we report development cardiac FRDA. In vivo heart imaging revealed profound impairments...

10.1093/hmg/ddt493 article EN Human Molecular Genetics 2013-10-08

Friedreich ataxia (FA), the most common inherited autosomal-recessive in Caucasians, is characterized by progressive degeneration of central and peripheral nervous system, hypertrophic cardiomyopathy increased incidence diabetes. FA caused a GAA repeat expansion first intron gene encoding frataxin, an evolutionarily conserved mitochondrial protein, which results decreased expression. Ubiquitous inactivation fly frataxin ortholog dfh blocks transition from larval to pupal stages. In this...

10.1093/hmg/ddv024 article EN Human Molecular Genetics 2015-01-26

fused (fu) is a segment-polarity gene encoding putative serine-threonine kinase. In wild-type context, all fu mutations display the same set of phenotypes. Nevertheless, Suppressor [Su(fu)] define three classes alleles (fuO, fuI, fuII). Here, we report molecular analysis known and generation new by in vitro mutagenesis. We show that Fused (Fu) protein functions vivo as The N-terminal kinase extreme C-terminal domains are necessary for Fu+ activity while central region appears to be...

10.1093/genetics/142.4.1181 article EN Genetics 1996-04-01

Proteins with long, pathogenic polyglutamine (polyQ) sequences have an enhanced propensity to spontaneously misfold and self-assemble into insoluble protein aggregates. Here, we identified 21 human proteins that influence polyQ-induced ataxin-1 misfolding proteotoxicity in cell model systems. By analyzing the of these modifiers, discovered a recurrent presence coiled-coil (CC) domains toxicity enhancers, while such were not present suppressors. This suggests CC contribute aggregation-...

10.1371/journal.pgen.1002897 article EN cc-by PLoS Genetics 2012-08-16
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