968 resultados para Scripta-elegans


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Report for the scientific sojourn carried out at the Columbia University, United States, from 2010 to 2012. Expression of SoxB genes correlates with the commitment of cells to a neural fate; however, the relevance of SoxB proteins in early vertebrate neurogenesis has been difficult to prove genetically due to embryonic lethality and presumed redundant functions. The nematode C. Elegants has only 5 sox genes: sox-2 and sox-3 form the SoxB group while sem-2, sox-4 and egl-13 belong to other Sox groups. Our results show that sox-2 and sem-2 are the sox genes expressed earliest and in a broader manner during embryogenesis, being expressed in several neuronal progenitors. sox-3, sox-4 and egl-13 are expressed in few cells during late embryogenesis, when most neurons are already born. Both sox-2 and sem-2 null mutants are early larval lethal but do not show neuronal specification defects during embryonic development as indicated by quantification of a panneuronal reporter. Potential redundancy or compensatory mechanisms between different sox genes have been ruled out, strongly suggesting that sox genes are not required for specification of embryonically-derived neurons. However, at the first larval stage there are still several blast cells that will give rise to different postembryonic lineages, which generate several neurons amongst other cell types. nterestingly, sox-2 is expressed in many of these progenitor cells. Using mosaic analysis we have so far identified neurons derived from two different postembryonic lineages which fail to be generated in C. elegans sox-2 mutants. These results support the idea that postembryonic progenitor competence is compromised in the absence of sox-2.

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Se efectuarón colecciones de "percebes" en diferentes localidades del área comprendida entre Yasila, Paita (05°08'S) y Chilca, Lima (12°29.5'S) identificándose los ejemplares como Pollicipes elegans, determinándose su distribución geográfica, densidad, talla, peso, la relación longitud-peso y algunos bioecológicos. También se recopilo información acerca de su extracción comercial.

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Presenta información sobre el estudio (cálculo y análisis) de la población y biomasa del percebes, realizado desde diciembre 1995 a diciembre 1997 en las áreas mencionadas. Brinda resultados que permiten medir las posibilidades de su explotación racional, considerando las variaciones estacionales y algunas condiciones biológicas.

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Presenta los resultados de la evaluación poblacional de percebes Pollicipes elegans en las islas Lobos de Afuera con el fin de estimar la magnitud del stock y determinar las características del recurso en relación al ambiente marino, como base para la toma de decisiones en su ordenamiento pesquero.

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Ordonnances et pièces diverses relatives au gouvernement du royaume, aux rapports de Philippe le Bel avec le Saint Siège, au grand schisme etc. F. 1, De origine singularum gentium,F. 104v, Notes sur divers événements du règne de Charles VI,F. 120, Glosa abbatis Joachim super libro Cirilli, F. 131v, Visio Johannis heremite, F. 137, Pavo, F. 140, Vincentii Ferrarii epistola de Antichristo, F. 167, Ordre de procéder en la ville et viconté de Paris, F. 194, Stilus curie parlamenti, editus per G. de Brolio, F. 255, Divers arrêts du Parlement,

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La distribución de tallas de pulpo fluctuó entre 40 y 200 mm de longitud del manto. El peso promedio fue 588,20 g, el 85% de los ejemplares no superó el peso mínimo de extracción (1 kg). En hembras predominaron estadios en desarrollo (63%), madurez total (16%); en machos predominaron estadios en desove (64%) y maduros (28%). La mayor concentración del recurso se registró al norte de la isla El Ladrón y frente a isla Quita Calcal. Las tallas de percebes fluctuaron entre 1 y 40 mm de longitud carina-rostral (Lcr), 55% de ejemplares estuvieron maduros. El percebes estuvo distribuido en el intermareal rocoso entre 6°56’9’’S y 6°57’30,6’’S en un área de 887,50 m2. La biomasa se estimó en 3,06 t ±27,18% y la población en 0,42 millones de individuos ±47,30%; el stock de juveniles (<17 mm) fue 0,17 millones de ejemplares; el stock adulto (≥17 mm) estuvo constituido por 0,24 millones de individuos y 2,90 t de la biomasa.

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Data sheet produced by the Iowa Department of Natural Resources is about different times of animals, insects, snakes, birds, fish, butterflies, etc. that can be found in Iowa.

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BACKGROUND: The human herpes simplex virus (HSV) host cell factor HCF-1 is a transcriptional coregulator that associates with both histone methyl- and acetyltransferases, and a histone deacetylase and regulates cell proliferation and division. In HSV-infected cells, HCF-1 associates with the viral protein VP16 to promote formation of a multiprotein-DNA transcriptional activator complex. The ability of HCF proteins to stabilize this VP16-induced complex has been conserved in diverse animal species including Drosophila melanogaster and Caenorhabditis elegans suggesting that VP16 targets a conserved cellular function of HCF-1. METHODOLOGY/PRINCIPAL FINDINGS: To investigate the role of HCF proteins in animal development, we have characterized the effects of loss of the HCF-1 homolog in C. elegans, called Ce HCF-1. Two large hcf-1 deletion mutants (pk924 and ok559) are viable but display reduced fertility. Loss of Ce HCF-1 protein at reduced temperatures (e.g., 12 degrees C), however, leads to a high incidence of embryonic lethality and early embryonic mitotic and cytokinetic defects reminiscent of mammalian cell-division defects upon loss of HCF-1 function. Even when viable, however, at normal temperature, mutant embryos display reduced levels of phospho-histone H3 serine 10 (H3S10P), a modification implicated in both transcriptional and mitotic regulation. Mammalian cells with defective HCF-1 also display defects in mitotic H3S10P status. CONCLUSIONS/SIGNIFICANCE: These results suggest that HCF-1 proteins possess conserved roles in the regulation of cell division and mitotic histone phosphorylation.

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Previous studies in Caenorhabditis elegans showed that RPM-1 (Regulator of Presynaptic Morphology-1) regulates axon termination and synapse formation. To understand the mechanism of how rpm-1 functions, we have used mass spectrometry to identify RPM-1 binding proteins, and have identified RAE-1 (RNA Export protein-1) as an evolutionarily conserved binding partner. We define a RAE-1 binding region in RPM-1, and show that this binding interaction is conserved and also occurs between Rae1 and the human ortholog of RPM-1 called Pam (protein associated with Myc). rae-1 loss of function causes similar axon and synapse defects, and synergizes genetically with two other RPM-1 binding proteins, GLO-4 and FSN-1. Further, we show that RAE-1 colocalizes with RPM-1 in neurons, and that rae-1 functions downstream of rpm-1. These studies establish a novel postmitotic function for rae-1 in neuronal development.

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The pathological formation of proteinaceous aggregates that accumulate into the brain cells of patients are hallmarks of neurodegenerative diseases such as Alzheimer's disease, amyotrophic lateral sclerosis and the heterogeneous group of polyglutamine (polyQ) diseases. In the polyQ diseases, the most upstream events of the pathogenic cascade are the misfolding and aggregation of proteins, such as huntingtin in Huntington's disease, that contain expanded stretch of glutamine residues above 35--‐40 repeats. This expanded polyQ stretch triggers the misfolding and aggregation of cytotoxic polyQ proteins in the neurons that cause cell death through different processes, like apoptosis, excessive inflammation, formation of free radicals, eventually leading to neuronal loss and neurodegeneration. This study focuses on the cellular network of chaperone proteins that can prevent protein aggregation by binding misfolding intermediates and may, as in the case of HSP70, actively unfold misfolded proteins into refoldable non--‐toxic ones (Hinault et al., 2010; Sharma et al., 2011). The chaperones can also collaborate with the proteasome to convert stable harmful proteins into harmless amino acids. Thus, the chaperone proteins that are the most important cellular factors of prevention and curing of protein misfolding, are negatively affected by aging (Morley et al., 2002) and fail to act properly in the neurons of aged persons, which eventually may lead to neurodegenerative pathologies. The general aim of this research was to identify least toxic drugs that can upregulate the expression of chaperone genes in cells suffering from polyQ--‐ mediated protein aggregation and degeneration. The specific aim of this study was to observe the effect of ten drugs on polyQ aggregation in a recombinant nematode Caenorhabditis elegans expressing a chimeric protein containing a sequence of 35 glutamines (Q35) fused to the green fluorescent protein in muscle cells, which causes an age--‐ and temperature--‐ dependent phenotype of accelerated paralysis. The drugs were selected after having proven their causing the overexpression of chaperone proteins in a previous wide screening of 2000 drugs on the moss plant Physcomitrella patens. The screening that we performed in this study was on these ten drugs. It suggested that piroxicam and anisindione were good reducers of polyglutamine disease mediated paralysis. A hypothesis can be made that they may act as good enhancers of the heat shock response, which causes the overexpression of many HSP chaperones and thus reduce motility impairment of polyQ disease expressing nematodes. Piroxicam was found to have the greatest effect on reducing polyQ35 proteins aggregates mediated paralysis in a dose--‐dependent manner but was also found to either have a toxic effect on wild type C.elegans, either to change its natural motility behavior, eventually reducing its motility in both cases. Chloroform should be preferred over DMSO as a drug solvent as it appears to be less toxic to C.elegans.