Nos tutelles


Nos partenaires

Accueil > Départements > Biologie Cellulaire > Jacques MONTAGNE : Croissance et Métabolisme

Publications de l’équipe


  • A. Arnal, C. Jacqueline, B. Ujvari, L. Leger, C. Moreno, D. Faugere, A. Tasiemski, C. Boidin-Wichlacz, D. Misse, F. Renaud, J. Montagne, A. Casali, B. Roche, F. Mery, et F. Thomas, « Cancer brings forward oviposition in the fly Drosophila melanogaster », Ecology and Evolution, vol. 7, nᵒ 1, p. 272-276, janv. 2017.
    Résumé : Hosts often accelerate their reproductive effort in response to a parasitic infection, especially when their chances of future reproduction decrease with time from the onset of the infection. Because malignancies usually reduce survival, and hence potentially the fitness, it is expected that hosts with early cancer could have evolved to adjust their life-history traits to maximize their immediate reproductive effort. Despite the potential importance of these plastic responses, little attention has been devoted to explore how cancers influence animal reproduction. Here, we use an experimental setup, a colony of genetically modified flies Drosophila melanogaster which develop colorectal cancer in the anterior gut, to show the role of cancer in altering life-history traits. Specifically, we tested whether females adapt their reproductive strategy in response to harboring cancer. We found that flies with cancer reached the peak period of oviposition significantly earlier (i.e., 2 days) than healthy ones, while no difference in the length and extent of the fecundity peak was observed between the two groups of flies. Such compensatory responses to overcome the fitness-limiting effect of cancer could explain the persistence of inherited cancer-causing mutant alleles in the wild.
    Mots-clés : BIOCELL, cancer, fecundity, life‐history strategy, METABO, reproduction.

  • P. Richards, S. Ourabah, J. Montagne, A. - F. Burnol, C. Postic, et S. Guilmeau, « MondoA/ChREBP: The usual suspects of transcriptional glucose sensing; Implication in pathophysiology », Metabolism: Clinical and Experimental, vol. 70, p. 133-151, mai 2017.
    Résumé : Identification of the Mondo glucose-responsive transcription factors family, including the MondoA and MondoB/ChREBP paralogs, has shed light on the mechanism whereby glucose affects gene transcription. They have clearly emerged, in recent years, as key mediators of glucose sensing by multiple cell types. MondoA and ChREBP have overlapping yet distinct expression profiles, which underlie their downstream targets and separate roles in regulating genes involved in glucose metabolism. MondoA can restrict glucose uptake and influences energy utilization in skeletal muscle, while ChREBP signals energy storage through de novo lipogenesis in liver and white adipose tissue. Because Mondo proteins mediate metabolic adaptations to changing glucose levels, a better understanding of cellular glucose sensing through Mondo proteins will likely uncover new therapeutic opportunities in the context of the imbalanced glucose homeostasis that accompanies metabolic diseases such as type 2 diabetes and cancer. Here, we provide an overview of structural homologies, transcriptional partners as well as the nutrient and hormonal mechanisms underlying Mondo proteins regulation. We next summarize their relative contribution to energy metabolism changes in physiological states and the evolutionary conservation of these pathways. Finally, we discuss their possible targeting in human pathologies.
    Mots-clés : BIOCELL, cancer, ChREBP, Diabetes, Glucose and lipid metabolism, METABO, MondoA.

  • F. Thomas, C. Jacqueline, T. Tissot, M. Henard, S. Blanchet, G. Loot, E. Dawson, F. Mery, F. Renaud, J. Montagne, C. Beckmann, P. A. Biro, R. Hamede, et B. Ujvari, « The importance of cancer cells for animal evolutionary ecology », Nature Ecology & Evolution, vol. 1, nᵒ 11, p. 1592-1595, nov. 2017.

  • F. Thomas, S. Rome, F. Mery, E. Dawson, J. Montagne, P. A. Biro, C. Beckmann, F. Renaud, R. Poulin, M. Raymond, et B. Ujvari, « Changes in diet associated with cancer: An evolutionary perspective », Evolutionary Applications, vol. 10, nᵒ 7, p. 651-657, août 2017.
    Résumé : Changes in diet are frequently correlated with the occurrence and progression of malignant tumors (i.e., cancer) in both humans and other animals, but an integrated conceptual framework to interpret these changes still needs to be developed. Our aim is to provide a new perspective on dietary changes in tumor-bearing individuals by adapting concepts from parasitology. Dietary changes may occur alongside tumor progression for several reasons: (i) as a pathological side effect with no adaptive value, (ii) as the result of self-medication by the host to eradicate the tumor and/or to slow down its progression, (iii) as a result of host manipulation by the tumor that benefits its progression, and finally (iv) as a host tolerance strategy, to alleviate and repair damages caused by tumor progression. Surprisingly, this tolerance strategy can be beneficial for the host even if diet changes are beneficial to tumor progression, provided that cancer-induced death occurs sufficiently late (i.e., when natural selection is weak). We argue that more data and a unifying evolutionary framework, especially during the early stages of tumorigenesis, are needed to understand the links between changes in diet and tumor progression. We argue that a focus on dietary changes accompanying tumor progression can offer novel preventive and therapeutic strategies against cancer.
    Mots-clés : BIOCELL, malignant cells, manipulation, METABO, nutrition, self‐medication, resistance, tolerance.



  • D. Garrido, T. Rubin, M. Poidevin, B. Maroni, A. Le Rouzic, J. - P. Parvy, et J. Montagne, « Fatty Acid Synthase Cooperates with Glyoxalase 1 to Protect against Sugar Toxicity », PLOS Genetics, vol. 11, nᵒ 2, p. e1004995, févr. 2015.
    Mots-clés : Animals, BIOCELL, Diabetes Mellitus, Type 2, Dietary Sucrose, Drosophila, Fatty Acid Synthase, Type I, Glycation End Products, Advanced, Humans, Insulin Resistance, Lactoylglutathione Lyase, Lipids, METABO, Metabolic Syndrome, Mutation, Neoplasms, Pyruvaldehyde, research support, non-u.s. gov't, Triglycerides.

  • C. Wicker-Thomas, D. Garrido, G. Bontonou, L. Napal, N. Mazuras, B. Denis, T. Rubin, J. - P. Parvy, et J. Montagne, « Flexible origin of hydrocarbon/pheromone precursors in Drosophila melanogaster », Journal of Lipid Research, vol. 56, nᵒ 11, p. 2094-2101, nov. 2015.
    Résumé : In terrestrial insects, cuticular hydrocarbons (CHCs) provide protection from desiccation. Specific CHCs can also act as pheromones, which are important for successful mating. Oenocytes are abdominal cells thought to act as specialized units for CHC biogenesis that consists of long-chain fatty acid (LCFA) synthesis, optional desaturation(s), elongation to very long-chain fatty acids (VLCFAs), and removal of the carboxyl group. By investigating CHC biogenesis in Drosophila melanogaster, we showed that VLCFA synthesis takes place only within the oenocytes. Conversely, several pathways, which may compensate for one another, can feed the oenocyte pool of LCFAs, suggesting that this step is a critical node for regulating CHC synthesis. Importantly, flies deficient in LCFA synthesis sacrificed their triacylglycerol stores while maintaining some CHC production. Moreover, pheromone production was lower in adult flies that emerged from larvae that were fed excess dietary lipids, and their mating success was lower. Further, we showed that pheromone production in the oenocytes depends on lipid metabolism in the fat tissue and that fatty acid transport protein, a bipartite acyl-CoA synthase (ACS)/FA transporter, likely acts through its ACS domain in the oenocyte pathway of CHC biogenesis. Our study highlights the importance of environmental and physiological inputs in regulating LCFA synthesis to eventually control sexual communication in a polyphagous animal.
    Mots-clés : Animals, BIOCELL, Biosynthetic Pathways, Drosophila melanogaster, Drosophila Proteins, Fat Body, fatty acid metabolism, Fatty Acid Synthase, Type I, Fatty Acids, Female, gene expression, Genetics, Homeostasis, Larva, Lipid droplets, Lipid Metabolism, lipoprotein receptors, Male, METABO, nutrition, Pheromones, Receptors, Lipoprotein, Triglycerides.
--- Exporter la sélection au format

Publications principales avant 2015

Parvy JP, P Wang, D Garrido, A Maria, C Blais, M Poidevin, J Montagne* 2014. Forward and Feedback Regulation of Cyclic Steroid Production in Drosophila melanogaster. Development, 141, 3955-65.

Mamai W, Mouline K, Parvy JP, Le Lannic J, Dabiré K R, Ouédraogo G A, Renault D, Frederic Simard 2014. Morphological changes in the spiracles of Anopheles gambiae sl (Diptera) as a response to the dry season conditions in Burkina Faso (West Africa). Parasit Vectors. 9:11 DOI 10.1186/s13071-015-1289-0.

Parvy JP, L Napal, T Rubin, M Poidevin, L Perrin, C Wicker-Thomas, J Montagne* 2012. Drosophila melanogaster Acetyl-CoA-Carboxylase Sustains a Fatty Acid-Dependent Remote Signal to Waterproof the Respiratory System. PLOS Genet 8 : e1002925.

Montagne J* 2011. More about Cyclin G from flies. Cell Cycle 10, 1187-8.

Montagne J*, C Lecerf, JP Parvy, JM Bennion, T Radimerski, ML Ruhf, F Zillbermann, N Vouilloz, E Hafen, S Kozma G Thomas 2010. A Novel Isoform of DHR3 Modulates dS6K-Dependent Growth. PLoS Genet 6(5) : e1000937.

Panic L, J Montagne, M Cokaric, S Volarevic 2007. S6-Haploinsufficiency Activates the p53 Tumor Suppressor. Cell Cycle 6, 20-4.

publié le , mis à jour le