Centre de Biologie du Développement

All Publications

MarcH — 2013-05-15T08:57:31Z

Arrivée d'Audrey Bellanger au service de gestion. Audrey est recrutée afin de renforcer le service jusqu'à la fin de cette année. Elle partagera son bureau avec Marion et Stéphanie.

Eric A — 2013-04-16T06:33:49Z

Vendredi 17 Mai à 11h salle Vandel . Roland Leborgne « Epithelial dynamics of cytokinesis in vivo ». Contact S Plaza

Eric A — 2013-04-15T06:02:45Z

- Informations

Ambre M. Bertholet, Aurélie M.E. Millet,Oriane Guillermin, Marlène Daloyau, Noélie Davezac, Marie-Christine Miquel and Pascale Belenguer (2013). OPA1 loss of function affects in vitro neuronal maturation. BRAIN

Eric A — 2013-04-10T08:49:42Z

Mitochondrial dynamics control the organelle's morphology, with fusion leading to the formation of elongated tubules and fission leading to isolated puncta, as well as mitochondrial functions. Recent reports have shown that disruptions of mitochondrial dynamics contribute to neurodegenerative diseases. Mutations of the inner membrane GTPase OPA1 are responsible for type 1 dominant optic atrophy (DOA), by mechanisms not fully understood. In murine cortical primary neurons, we show here that down-regulation of the OPA1 protein leads to fragmented mitochondria that become less abundant along the dendrites. Furthermore, this inhibition results in reduced expression of mitochondrial respiratory complexes as well as mitochondrial DNA, decreased mitochondrial membrane potential, and diminished ROS levels. The onset of synaptogenesis was markedly impaired via reductions in pre- and post-synaptic structural protein expression and synapses number without first affecting the dendritic arborization. With longer time in culture, OPA1 extinction led to a major restriction of dendritic growth, together with synaptic proteins reduction. Furthermore, in maturing neurons we observed a transitory increase in mitochondrial filament length, associated with marked changes in the expression levels of OPA1, which occurred at the onset of synaptogenesis simultaneously to transitory increase in ROS levels and NRF2 nuclear translocation. This observation suggests that mitochondrial hyperfilamentation acts upstream of a ROS-dependent NRF2 transcriptional activity, possibly impacting neuronal maturation, such a process being impaired by insufficient amount of OPA1. Altogether, our findings suggest a new role for OPA1 in synaptic maturation and dendritic growth through maintenance of proper mitochondrial oxidative metabolism and distribution, highlighting the role of mitochondrial dynamics in neuronal functioning and providing insights into DOA pathogenesis, since OPA1 loss affecting neuronal maturation could lead to early synaptic dysfunctions.

Vulgarisation Scientifique au CBD les jeudi 4 et vendredi 5 avril 2013

Eric A — 2013-04-05T07:44:01Z

Deux types de visite ont eu lieu : celle de professeurs du secondaire sur une journée de formation continue intitulée "Profs en labo" proposée par le rectorat ainsi que celle d'élèves de seconde du lycée de Fronton dans le cadre d'un projet bi-disciplinaire Math-Biologie. Ce projet a débuté par une série de travaux pratiques sur la drosophile au lycée alliant génétique et statistiques et s'est finalisé par la visite d'un laboratoire de recherche en Biologie (CBD) et en Mathématiques (IMT) à l'Université . Élèves et professeurs ont pu appréhender certaines problématiques de la recherche fondamentale et découvrir les différents métiers qui lui sont associés. Ils ont également découvert la palette de modèles animaux utilisés de façon complémentaire pour l'analyse d'une question biologique, ainsi que les derniers développements techniques concernant notamment l'imagerie.

Ephrin-B1 maintains apical adhesion of neural progenitors (2013) Dina N. Arvanitis, Annie Béhar, Petra Tryoen-Tóth, Jeff O. Bush, Thomas Jungas, Nicolas Vitale and Alice Davy. Development.

Eric A — 2013-03-10T16:45:00Z

Apical neural progenitors are polarized cells whose apical membrane is the site of cell-cell and cell-extracellular matrix adhesion events that are essential to maintain the integrity of the developing neuroepithelium. Apical adhesion is important for several aspects of the nervous system development including morphogenesis and neurogenesis, yet the mechanisms underlying its regulation remain poorly understood. Herein, we show that ephrin-B1, a cell surface protein that engages in cell signaling upon binding cognate Eph receptors, controls normal morphogenesis of the developing cortex. Efnb1 deficient embryos exhibit morphological alterations of the neuroepithelium which correlate with neural tube closure defects. Using loss-of-function experiments by ex vivo electroporation we demonstrate that ephrin-B1 is required in APs to maintain their apical adhesion. Mechanistically, we show that ephrin-B1 controls cell/ECM adhesion by promoting apical localization of integrin-1 and we identify ADP-ribosylation factor 6 (ARF6) as an important effector of ephrin-B1 reverse signaling in apical adhesion of APs. Our results provide evidence for an important role for ephrin-B1 in maintaining the structural integrity of the developing cortex and highlight the importance of tightly controlling apical cell/ECM adhesion for neuroepithelial development.

Kioske Dimanche 3 Mars

Eric A — 2013-02-21T08:37:00Z

En préambule à la semaine du cerveau qui se déroulera du 11 au 17 Mars, le Kiosque Actus du 3 Mars sera consacré à deux modèles biologiques qui aident à mieux comprendre certains aspects du cerveau : l'abeille pour l'étude de l'odorat et la souris pour l'étude de la mémoire. C'est Dimanche, c'est gratuit.

Bibonne A, Néant I, Batut J, Leclerc C, Moreau M, Gilbert T. (2012) ]Three calcium-sensitive genes, fus, brd3 and wdr5, are highly expressed in neural and renal territories during amphibian development. Biochim Biophys Acta.

Eric A — 2013-01-15T08:59:22Z

Numerous Ca2+ signaling events have been associated with early development of vertebrate embryo, from fertilization to organogenesis. In Xenopus laevis, Ca2+ signals are key regulators in the earliest steps of the nervous system development. If neural determination is one of the best-characterized examples of the role of Ca2+ during embryogenesis, increasing literature supports a determining role of organogenesis and differentiation. In blastula the cells of the presumptive ectoderm (animal caps) are pluripotent and can be induced toward neural fate with an intracellular increase of free Ca2+ triggered by caffeine. To identify genes that are transcribed early upon Ca2+ stimuli and involved in neural determination, we have constructed a subtractive cDNA library between neuralized and non-neuralized animal caps. Here we present the expression pattern of three new Ca2+-sensitive genes: fus (fused in sarcoma), brd3 (bromodomain containing 3) and wdr5 (WD repeat domain 5) as they all represent potential regulators of the transcriptional machinery. Using in situ hybridization we illustrated the spatial expression pattern of fus, brd3 and wdr5 during early developmental stages of Xenopus embryos. Strikingly, their domains of expression are not restricted to neural territories. They all share a specific expression throughout renal organogenesis which has been found to rely also on Ca2+ signaling. This therefore highlights the key function of Ca2+ target genes in specific territories during early development. We propose that Ca2+ signaling through modulation of fus, brd3 and wdr5 expressions can control the transcription machinery to achieve proper embryogenesis.

« Le CBD organise ses journées scientifiques les 6 et 7 mai 2013 au Muséum d'Histoire Naturelle de Toulouse. Ces journées permettront aux chercheurs du laboratoire de présenter leurs dernieres avancées scientifiques et de discuter sur les perspectives de leurs travaux».

Eric A — 2013-01-09T14:35:24Z

Présentation des avancées scientifiques effectuées et discussion sur les perspectives

Sulfatase 1 promotes the motoneuron to oligodendrocyte fate switch by activating Shh signalling in Olig2 progenitors of the embryonic ventral spinal cord

Eric A — 2012-10-22T12:49:52Z

Yacine Touahri, Nathalie Escalas, Bertrand Benazeraf, Philippe Cochard, Cathy Danesin and Cathy Soula. Journal of Neuroscience (2012)

In the developing ventral spinal cord, motor neurons (MNs) and oligodendrocyte precursor cells (OPCs) are sequentially generated from a common pool of neural progenitors included in the so called pMN domain characterized by Olig2 expression. Here, we establish that the secreted Sulfatase 1 (Sulf1) is a major component of the mechanism that causes these progenitors to stop producing MNs and change their fate to generate OPCs. We show that specification of OPCs is severely affected in sulf1-deficient mouse embryos. This defect does not rely on abnormal patterning of the spinal cord or failure in maintenance of pMN progenitors at the onset of OPC specification. Instead, the efficiency of OPC induction is reduced, only few Olig2 progenitors are recruited to generate OPCs, meanwhile they continue to produce MNs beyond the normal timing of the neuroglial switch. Using the chicken embryo, we show that Sulf1 activity is required precisely at the stage of the MN to OPC fate switch. Finally, we bring arguments supporting the view that Sulf1 controls the level of Shh signalling activity, behaving as an enhancer rather than an obligatory component in the Shh pathway. Our study provides additional insights into the temporal control of Olig2 progenitor cell fate change by the identification of Sulf1 as an extracellular timing signal in the ventral spinal cord.