Evaluación de la población del percebes Pollicipes elegans en las islas Lobos de Afuera (18 - 20 julio 2001)

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.

Islas Lobos de Afuera: Evaluación de pulpo Octopus mimus Gould, 1852 y percebes Pollicipes elegans (Lesson, 1831), Lambayeque, 2010

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.

King Rail Rallus Elegans, 2011

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.

Epigenetic regulation of histone H3 serine 10 phosphorylation status by HCF-1 proteins in C. elegans and mammalian cells.

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.

RAE-1, a novel PHR binding protein, is required for axon termination and synapse formation in Caenorhabditis elegans.

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.

Motility tests for drugs preventing PolyQ aggregation in recombinant Caenorhabditis elegans.

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.

Functional GacS in Pseudomonas DSS73 prevents digestion by Caenorhabditis elegans and protects the nematode from killer flagellates.

The success of biocontrol bacteria in soil depends in part on their ability to escape predation. We explored the interactions between Pseudomonas strain DSS73 and two predators, the nematode Caenorhabditis elegans and the flagellate Cercomonas sp. Growth of the nematode in liquid culture was arrested when it was feeding on DSS73 or a DSS73 mutant (DSS73-15C2) unable to produce the biosurfactant amphisin, whereas a regulatory gacS mutant (DSS73-12H8) that produces no exoproducts supported fast growth of the nematode. The flagellate Cercomonas sp. was able to grow on all three strains. The biosurfactant-deficient DSS73 mutant caused severe dilation of the nematode gut. In three-species systems (DSS73, Cercomonas and C. elegans), the nematodes fed on the flagellates, which in turn grazed the bacteria and the number of C. elegans increased. The flagellates Cercomonas sp. usually kill C. elegans. However, DSS73 protected the nematodes from flagellate killing. Soil microcosms inoculated with six rhizobacteria and grazed by nematodes were colonized more efficiently by DSS73 than similar systems grazed by flagellates or without grazers. In conclusion, our results suggest that C. elegans and DSS73 mutually increase the survival of one another in complex multispecies systems and that this interaction depends on the GacS regulator.

Mouse Grueneberg ganglion neurons share molecular and functional features with C. elegans amphid neurons.

The mouse Grueneberg ganglion (GG) is an olfactory subsystem located at the tip of the nose close to the entry of the naris. It comprises neurons that are both sensitive to cold temperature and play an important role in the detection of alarm pheromones (APs). This chemical modality may be essential for species survival. Interestingly, GG neurons display an atypical mammalian olfactory morphology with neurons bearing deeply invaginated cilia mostly covered by ensheathing glial cells. We had previously noticed their morphological resemblance with the chemosensory amphid neurons found in the anterior region of the head of Caenorhabditis elegans (C. elegans). We demonstrate here further molecular and functional similarities. Thus, we found an orthologous expression of molecular signaling elements that was furthermore restricted to similar specific subcellular localizations. Calcium imaging also revealed a ligand selectivity for the methylated thiazole odorants that amphid neurons are known to detect. Cellular responses from GG neurons evoked by chemical or temperature stimuli were also partially cGMP-dependent. In addition, we found that, although behaviors depending on temperature sensing in the mouse, such as huddling and thermotaxis did not implicate the GG, the thermosensitivity modulated the chemosensitivity at the level of single GG neurons. Thus, the striking similarities with the chemosensory amphid neurons of C. elegans conferred to the mouse GG neurons unique multimodal sensory properties.

The role of PLK-1 in asynchronous cell division of two-cell stage "C. elegans" embryos

Summary Acquisition of lineage-specific cell cycle duration is an important feature of metazoan development. In Caenorhabditis a/egans, differences in cell cycle duration are already apparent in two-cell stage embryos, when the larger anterior blastomere AB divides before the smaller posterior blastomere P1. This time difference is under the control of anterior-posterior (A-P) polarity cues set by the PAR proteins. The mechanism by which these cues regulate the cell cycle machinery differentially in AB and P1 are incompletely understood. Previous work established that retardation of P1 cell division is due in part to preferential activation of an ATL1/CHK-1 dependent checkpoint in P1 but how the remaining time difference is controlled was not known at the onset of my work. The principal line of work in this thesis established that differential timing relies also on a mechanism that promotes mitosis onset preferentially in AB. The polo-like kinase PLK-1, a positive regulator of mitotic entry, is distributed in an asymmetric manner in two-cell stage embryos, with more protein present in AB than in P1. We find that PLK-1 asymmetry is regulated by anterior-posterior (A-P) polarity cues through preferential protein retention in the embryo anterior. Importantly, mild inactivation of plk-1 by RNAi delays entry into mitosis in P1 but not in AB, in a manner that is independent of ATL-1/CHK-1. Together, these findings favor a model in which differential timing of mitotic entry in C. elegans embryos relies on two complementary mechanisms: ATL-1/CHK-1 dependent preferential retardation in P1 and PLK-1 dependent preferential promotion in AB, which together couple polarity cues and cell cycle progression during early development. Besides analyzing PLK-1 asymmetry and its role in differential timing of two-cells stage embryos, we also characterized t2190, a mutant that exhibits reduced differential timing between AB and P1. We found this mutant to be a new allele of par-1. Additionally, we analyzed the role of NMY-2 in regulating the asynchrony of two-cell stage embryos, which may be uncoupled from its role in A-P polarity establishment and carried out a preliminary analysis of the mechanism underlying CDC-25 asymmetry between AB and P,. Overall, our works bring new insights into the mechanism controlling cell cycle progression in early C. elegans embryos. As most of the players important in C. elegans are conserved in other organisms, analogous mechanisms may be utilized in polarized cells of other species. Résumé Au cours du développement, les processus de division cellulaire sont régulés dans l'espace et le temps afin d'aboutir à la formation d'un organisme fonctionnel. Chez les Métazoaires, l'un des mécanismes de contrôle s'effectue au niveau de la durée du cycle cellulaire, celle-ci étant specifiée selon la lignée cellulaire. L'embryon du nématode Caenorhabditis elegans apparaît comme un excellent modèle d'étude de la régulation temporelle du cycle cellulaire. En effet, suite à la première division du zygote, l'embryon est alors composé de deux cellules de taille et d'identité différentes, appelées blastomères AB et P1. Ces deux cellules vont ensuite se diviser de manière asynchrone, le grand blastomère antérieur AB se divisant plus rapidement que le petit blastomère postérieur P1. Cette asynchronie de division est sous le contrôle des protéines PAR qui sont impliquées dans l'établissement de l'axe antéro-postérieur de l'embryon. A ce jour, les mécanismes moléculaires gouvernant ce processus d'asynchronie ne sont que partiellement compris. Des études menées précédemment ont établit que le retard de division observé dans le petit blastomère postérieur P1 était dû, en partie, à l'activation préférentielle dans cette cellule de ATL-1/CHK-1, protéines contrôlant la réponse à des erreurs dans le processus de réplication de l'ADN. L'analyse des autres mécanismes responsables de la différence temporelle d'entrée en mitose des deux cellules a été entreprise au cours de cette thèse. Nous avons considéré la possibilité que l'asynchronie de division était du à l'entrée préférentielle en mitose du grand blastomère AB. Nous avons établi que la protéine kinase PLK-1 (polo-like kinase 1), impliquée dans la régulation positive de la mitose, était distribuée de manière asymétrique dans l'embryon deux cellules. PLK-1 est en effet enrichi dans le blastomère AB. Cette localisation asymétrique de PLK-1 est sous le contrôle des protéines PAR et semble établie via une rétention de PLK-1 dans la cellule AB. Par ailleurs, nous avons démontré que l'inactivation partielle de plk-7 par interférence à ARN (RNAi) conduit à un délai de l'entrée en mitose de la cellule P1 spécifiquement, indépendamment des protéines régulatrices ATL-1/CHK-1. En conclusion, nous proposons un modèle de régulation temporelle de l'entrée en mitose dans l'embryon deux cellules de C. elegans basé sur deux mécanismes complémentaires. Le premier implique l'activation préférentielle des protéines ATL-1/CHK-1, et conduit à un retard d'entrée en mitose spécifiquement dans la cellule P1. Le second est basé sur la localisation asymétrique de la protéine kinase PLK-1 dans la cellule AB et induit une entrée précoce en mitose de cette cellule. Par ailleurs, nous avons étudié un mutant appelé t2190 qui réduit la différence temporelle d'entrée en mitose entre les cellules AB et P1. Nous avons démontré que ce mutant correspondait à un nouvel allèle du Bene par-1. De plus, nous avons analysé le rôle de NMY-2, une protéine myosine qui agit comme moteur moléculaire sur les filaments d'active; dans la régulation de l'asynchronie de division des blastomères AB et P1, indépendamment de sa fonction dans l'établissement de l'axe antéro-postérieur. Par ailleurs, nous avons commencé l'étude du mécanisme moléculaire régulant la localisation asymétrique entre les cellules AB et P1 de la protéine phosphatase CDC25, qui est également un important régulateur de l'entrée en mitose. En conclusion, ce travail de thèse a permis une meilleure compréhension des mécanismes gouvernant la progression du cycle cellulaire dans l'embryon précoce de C. elegans. Etant donné que la plupart des protéines impliquées dans ces processus sont conservées chez d'autres organismes multicellulaires, il apparaît probable que les mécanismes moléculaires révélés dans cette étude soit aussi utilisés chez ceux-ci.

Translation of polarity cues into asymmetric spindle positioning in "Caenorhabditis elegans"

Abstract: Asymmetric cell division is important to generate tissue diversity. The Caenorhabditis elegans embryo is well suited to study the mechanisms of asymmetric cell division. In wild type one-cell stage embryos, the spindle sets up along the anterior-posterior axis (AP). During anaphase, the spindle elongates. While the anterior spindle pole is relatively immobile, the posterior spindle pole moves towards the posterior cortex during anaphase leading to an asymmetric spindle position. As a result, the first cleavage gives rise to a large anterior blastomere and a smaller posterior one, which differs also in cell fate determinants. This posterior spindle displacement occurs in response to polarity cues set up along the AP axis by the PAR proteins and is due to imbalanced pulling forces acting on the two spindle poles, with net forces acting on the posterior spindle pole being more extensive than those at the anterior one. The project of my thesis was to characterize the involvement of two new components, gpr-1 and gpr-2, in spindle positioning. These genes encode essentially identical proteins containing a GoLoco motif characteristic of proteins interacting with α subunits of heterotrimeric G protein (Gα). In gpr-1/2(RNAi) embryos and in embryos lacking simultaneously two α subunits, goa-1 and gpa-16, (Ga(RNAi) embryos), there is a minimal posterior displacement of the spindle during anaphase, and the first division is equal. I found that the pulling forces acting on the two spindle poles is weak and equal in gpr-1/2(RNAi) and Gα (RNAi) embryos. I found that GPR-1/2 acts downstream of polarity cues for generation of pulling forces. Furthermore, I showed that GPR-1/2 distribution was enriched at the posterior cortex during metaphase whereas GOA-1 and GPA-16 were uniformly distributed at the cell cortex throughout the cell cycle. Gα subunits oscillate between GDP- and GTP-bound forms. Gα signaling is turned on by GDP/GTP exchange catalyzed by guanine nucleotide exchange factors (GEFs) and turned off by hydrolysis of GTP catalyzed by GTPase activating proteins (GAPs). A third class of proteins, the guanine dissociation inhibitors (GDIs), binds the GDP-bound form of Gα subunits and inhibits nucleotide exchange. I found that GPR-1/2 acts as a GDI for GOA-1. Taken together, my findings suggest a model in which differential activation of Gα subunits along the AP axis may translate into generation of differential pulling forces on the anterior and posterior spindle poles, and, thus, asymmetric cell division. Résumé L'embryon du nématode Caenorhabditis elegans est un modèle approprié pour étudier les mécanismes de la division asymétrique. Chez l'embryon précoce, le fuseau mitotique se forme le long de l'axe antéro-postérieur (A/P) et au centre de l'embryon, le pôle antérieur restant relativement immobile alors que le pôle postérieur du fuseau se déplace vers le cortex postérieur au cours de l'anaphase conduisant à une position excentrée du fuseau. 11 en résulte une première division qui génère un blastomère antérieur et postérieur de grande et petite taille respectivement et qui diffèrent en facteurs développementaux. Ce déplacement postérieur se produit en réponse de la polarité établie par la distribution polarisée des protéines PAR et est le résultat de la génération de forces inégales tirant sur les deux pôles du fuseau, les forces agissant sur le pôle postérieur du fuseau étant plus grandes. Le projet de ma thèse était d'identifier la fonction de deux nouveaux constituants, gpr-1 et gpr-2 dans le positionnement asymétrique du fuseau. Ces gènes codent essentiellement pour la même protéine qui contient un motif GoLoco, caractéristique des protéines interagissant avec la sous-unité alpha des protéines G hétérotrimériques. Chez l'embryon gpr-1/2(RNAi) et chez les embryons dépourvus d'activité de deux sous-unités alpha, goa-1 et gpa-16, (Gα(RNAi)), j'ai montré qu'il y avait un déplacement minimal du fuseau vers le pôle postérieur au cours de l'anaphase et la première division est symétrique en raison de forces faibles et égales agissant sur les deux pôles du fuseau. J'ai également montré que gpr-1/2 était requis en aval des signaux établissant la polarité pour générer les forces responsables du positionnement asymétrique du fuseau. De plus, j'ai montré que GPR-1/2 était enrichi au pôle postérieur lors de la métaphase alors que GOA-1 et GPA-16 étaient localisés de façon uniforme au cortex de l'embryon précoce. Gas oscillent entre une forme liée au GDP et une forme liée au GTP. La signalisation des Gas est activée par l'échange GDP/GTP qui est catalysé par des protéines GEFs. La signalisation des Gas est désactivée par l'hydrolyse du GTP qui est catalysée par des protéines GAPs. Une troisième classe de protéines, GDIs lie la forme GDP et inhibe l'échange de nucléotides. J'ai montré que GPR-1/2 agissait comme un GDI pour GOA-1. Mes résultats suggèrent un modèle dans lequel une activation différentielle des Gα le long de l'axe A/P pourrait générer des forces différentielles sur le pôle antérieur et postérieur du fuseau.

Constituintes químicos e atividade inseticida dos extratos de frutos de Trichilia elegans E T. catigua (Meliaceae)

Phytochemical investigation of the fruits extracts of Trichilia elegans and Trichilia catigua (Meliaceae) has led to the identification of the limonoids 11β-acetoxyobacunone, cedrelone, methylangolensate and epimeric mixture of photogedunin besides known coumarins (scoparone, scopoletin, umbeliferone) and the steroids stigmasterol, β-sitosterol, sitostenone and campesterol. The structures of the compounds were proposed by spectroscopic analysis and comparison with literature data. An evaluation of the insecticidal activity of the fruits extracts of Trichilia ssp. was carried out and the extracts of T. elegans revealed to have strong insecticidal activity and the extracts of T. catigua showed moderate larval mortality on Spodoptera frugiperda.

To kompson sive ide qvod variâ ratione elegans est & dicitur

Invocatio: Secundante Deo! - Ded.: Johannes Gezelius, Georgius Biugg, Martinus Rivelius, Jacobus Werander, Ericus Essevius, Jacobus Haustrammius, Carolus Hoffreen.

Ocorrência de podridão negra, causada por Chalara elegans, em raízes de cenoura no Rio Grande do Sul

A black root rot in carrot (Daucus carotae), caused by Chalara elegans, is reported for the first time in the State of Rio Grande do Sul, Brazil.

Dispersão de sementes de uruvalheira (Platypodium elegans vog.) (Fabaceae) em um cerradão, Uberlândia-MG

Estudou-se a dispersão de sementes de cinco árvores-matriz de Platypodium elegans Vog. (Fabaceae) em área de cerradão, na Estação Ecológica do Panga (EEP). As amostragens foram feitas em parcelas de 0,25 m2, posicionadas em linhas partindo da base da matriz em direção aos quatro pontos cardeais (Norte, Sul, Leste e Oeste), marcadas a cada metro. No laboratório, os frutos foram abertos para análise da qualidade das sementes. Foram amostradas 1.131 sementes, das quais 18,4% estavam intactas e 81,6%, danificadas e provavelmente inviáveis para germinação. A dispersão das sementes sofreu influência da topografia do local das matrizes, das respostas fisiológicas e genéticas à pré-dispersão, bem como do possível direcionamento favorável do vento. Dessa forma, a atuação conjunta desses fatores funcionaria como facilitadores relevantes na formação do banco de sementes e moldaria a probabilidade de estabelecimento de novos indivíduos, tanto na área estudada quanto nas fisionomias adjacentes..

Kvalitet elegans ekonomi styrka

kuv., 22 x 18 cm