Analyse et géométrie, histoire des courbes gauches De Clairaut à Darboux

Cet article est consacré à l’histoire de la théorie locale des courbes “à double courbure”. Initiée par Clairaut en 1731, cette théorie se développe en parallèle à la théorie des surfaces et trouve son achèvement avec les formules de Serret et Frenet et leur interprétation par Darboux, en 1887. Au delà de l’analyse des contributions de nombreux mathématiciens, parmi lesquels Monge bien s?r mais aussi Fourier, Lagrange et Cauchy, notre étude donne un regard particulier sur l’évolution conjointe de l’Analyse et de la Géométrie, dans une longue période riche de nombreuses remises en cause théoriques.     

The SH3-binding domain of Cx43 participates in loop/tail interactions critical for Cx43-hemichannel activity

Connexin 43 (Cx43) hemichannels establish local signaling networks via the release of ATP and other molecules, but their excessive opening may result in cell death. Hence, the activity of Cx43-hemichannels ought to be critically controlled. This involves interactions between the C-terminal tail (CT) and the cytoplasmic loop (CL), more particularly the L2 domain within CL. Previous work revealed an important role for the last nine amino acids of the Cx43 CT by targeting the L2 domain, as these nine amino acids were sufficient to restore the activity of CT-truncated Cx43-hemichannels. However, we discovered that deletion of the last 19 amino acids of the CT only partially lowered the binding to the L2 domain, indicating that a second L2-binding region is present in the CT. We here provide evidence that the SH3-binding domain is another CT region that targets the L2 domain. At the functional level, the SH3-binding domain was able to restore the activity of CT-truncated Cx43-hemichannels and alleviate the inhibition of full-length Cx43-hemichannels by high intracellular Ca²⁺ concentration ([Ca²⁺]_i) as demonstrated by various approaches including patch clamp studies of unitary Cx43-hemichannel activity. Finally, we show that in full-length Cx43-hemichannels, deletion of either the SH3-binding domain or the CT9 region suppresses the hemichannel activity, while deletion of both domains completely annihilates the hemichannel activity. These results demonstrate that the Cx43 SH3-binding domain, in addition to the CT9 region, critically controls hemichannel activity at high [Ca²⁺]_i, which may be involved in pathological hemichannel opening.     

Aspects biochimiques de la Régénération

Summary A survey of the biochemistry of regenerating animals has been made: after a critical discussion ofChild's metabolic gradients theory, the relative importance of respiration rate, carbohydrates, proteins and nucleic acids metabolism are stressed. The similarities between biochemical processes in the embryo and the regenerating organism are pointed out.

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Une grande partie de cet article est la reproduction d'un chapitre de notre livre « Embryologie chimique » (Masson, Paris, etDesoer, Liége); nous tenons à remercier les éditeurs de l'ouvrage qui ont bien voulu marquer leur accord. On y trouvera une bibliographie étendue sur les modifications chimiques dont l'organisme en régénération est le siège.     

Assembléegénérale de l'Union Radio-Scientifique Internationale (URSI) à Paris

Sans résumé     

Desiccation in the black dragon,Hagenius brevistylus Selys

Summary Hagenius brevistylus lost mass by evaporation in a moderately desiccating environment at the rate of 20.4 mg h^–1, and died of desiccation in less than 1 day at a body mass of 79.8% of their normally hydrated mass. It was estimated thatHagenius minimally would have to consume the equivalent of 60% of its body mass each day to meet its daily water requirements. This amount of food is equivalent to that necessary to power flight of a dragonfly for 4.6h.This research was financed in part by a grant from the American Philosophical Society to C.R.T., and was conducted at the University of Michigan Biological Station, Douglas Lake (USA).     

Senataxin, the ortholog of a yeast RNA helicase, is mutant in ataxia-ocular apraxia 2

Ataxia-ocular apraxia 2 (AOA2) was recently identified as a new autosomal recessive ataxia. We have now identified causative mutations in 15 families, which allows us to clinically define this entity by onset between 10 and 22 years, cerebellar atrophy, axonal sensorimotor neuropathy, oculomotor apraxia and elevated alpha-fetoprotein (AFP). Ten of the fifteen mutations cause premature termination of a large DEAxQ-box helicase, the human ortholog of yeast Sen1p, involved in RNA maturation and termination.     

Investigations on the toxic action ofAmanita phalloides Fr. on the hepatic cell

Riassunto Nel ratto intossicato con estratto diAmanita phalloide le prime alterazioni strutturali dell'epatocita si realizzano a livello del nucleo e del nucleolo con formazioni di «nucleolar caps». Da queste stesse strutture iniziano i fenomeni di regressione delle alterazioni. Le manifestazioni sia del danno che della sua regressione a livello citoplasmatico risultano essere successive a quelle nucleari. Il comportamento del DNA e di alcuni enzimi del tessuto epatico è risultato nel complesso coerente con le alterazioni morfologiche. In rapporto con la dose usata queste alterazioni risultano reversibili poichè nelle cellule colpite entro 12 h cominciano i fenomeni di ristrutturazione.     

The K-Cl cotransporter KCC3 is mutant in a severe peripheral neuropathy associated with agenesis of the corpus callosum

Peripheral neuropathy associated with agenesis of the corpus callosum (ACCPN) is a severe sensorimotor neuropathy associated with mental retardation, dysmorphic features and complete or partial agenesis of the corpus callosum. ACCPN is transmitted in an autosomal recessive fashion and is found at a high frequency in the province of Quebec, Canada. ACCPN has been previously mapped to chromosome 15q. The gene SLC12A6 (solute carrier family 12, member 6), which encodes the K+-Cl- transporter KCC3 and maps within the ACCPN candidate region, was screened for mutations in individuals with ACCPN. Four distinct protein-truncating mutations were found: two in the French Canadian population and two in non-French Canadian families. The functional consequence of the predominant French Canadian mutation (2436delG, Thr813fsX813) was examined by heterologous expression of wildtype and mutant KCC3 in Xenopus laevis oocytes; the truncated mutant is appropriately glycosylated and expressed at the cellular membrane, where it is non-functional. Mice generated with a targeted deletion of Slc12a6 have a locomotor deficit, peripheral neuropathy and a sensorimotor gating deficit, similar to the human disease. Our findings identify mutations in SLC12A6 as the genetic lesion underlying ACCPN and suggest a critical role for SLC12A6 in the development and maintenance of the nervous system.     

A myogenic differentiation checkpoint activated by genotoxic stress

Cell-cycle checkpoints help to protect the genomes of proliferating cells under genotoxic stress. In multicellular organisms, cell proliferation is often directed toward differentiation during development and throughout adult homeostasis. To prevent the formation of differentiated cells with genetic instability, we hypothesized that genotoxic stress may trigger a differentiation checkpoint. Here we show that exposure to genotoxic agents causes a reversible inhibition of myogenic differentiation. Muscle-specific gene expression is suppressed by DNA-damaging agents if applied prior to differentiation induction but not after the differentiation program is established. The myogenic determination factor, MyoD (encoded by Myod1), is a target of the differentiation checkpoint in myoblasts. The inhibition of MyoD by DNA damage requires a functional c-Abl tyrosine kinase (encoded by Abl1), but occurs in cells deficient for p53 (transformation-related protein 53, encoded by Trp53) or c-Jun (encoded by the oncogene Jun). These results support the idea that genotoxic stress can regulate differentiation, and identify a new biological function for DNA damage-activated signaling network.