Overblog Suivre ce blog
Administration Créer mon blog
Bioécologie

Articles avec #organismes de laboratoire

Daphnia pulex Genome

4 Février 2011,

Publié par JMB

"The water flea, Daphnia, represents a major taxonomic lineage of aquatic arthropod diversity. Colbourne et al. (p. 555; see the Perspective by Ebert) present Daphnia's tiny genome, which nevertheless contains a large inventory of genes with many duplicated genes and expanded gene families that lack homology to genes in other sequenced genomes."

Source: Science 4 February 2011

 

AlgaeBase

27 Janvier 2010,

Publié par JMB

What is AlgaeBase?

AlgaeBase is a database of information on algae that includes terrestrial, marine and freshwater organisms. At present, the data for the marine algae, particularly seaweeds, are the most complete. For convenience, we have included the sea-grasses even though they are flowering plants.

Limitations

AlgaeBase is often a compromise of taxonomic opinions that may or may not reflect your particular conclusions. It is also a work in progress, and much of the data is incomplete. Feel free to use the information and images included here, but do please cite AlgaeBase in your publications or presentations. This helps to raise money in order to maintain the service. Please also realise that AlgaeBase is made available in its incomplete form and is purely meant as a aid to taxonomic studies and not a definitive source in its own right. You should always check the information included prior to use.

Contributors

Many organisations and people have, funded supported and contributed to AlgaeBase since its small beginnings on 20 March 1996. A full list is here.

More informations here

Chironomus riparius en écotoxicologie

8 Janvier 2010,

Publié par JMB

Chironomus-adulte-et-Nelly-Dal-Pos.jpgParmi les macro-invertébrés benthiques, Chironomus riparius est une espèce modèle communément utilisée en écotoxicologie pour évaluer la toxicité du sédiment (à gauche, une photo d'adultes). En effet, les raisons motivant son utilisation sont : (1) son ubiquité et son abondance (Environnement Canada, 1997), (2) son rôle-clé dans la structure et le fonctionnement des écosystèmes aquatiques, (3) son contact direct avec le sédiment lors des phases de développement larvaire (Goodyear K.L. et McNeill S., 1999, Thomas P. et Liber K., 2001), (4) sa relative facilité d’élevage en condition de laboratoire (Environnement Canada, 1997, OECD, 2001), (5) son cycle de vie - d'une durée totale de 20 à 30 jours à 21°C - permettant l'étude de scenarii d’exposition chronique d’une ou plusieurs générations, sur une période relativement courte.

Son cycle de vie se décompose en quatre stades de développement : l’œuf, la larve, la nymphe et l’imago (Armitage et al., 1995).

Les femelles chironomes pondent une série d’œufs enrobés d’un manteau mucilagineux appelé masse. Une femelle ne pond qu’une masse d’œuf au cours de sa vie (Ducrot V., 2005). Après l’éclosion des œufs, les larves restent dans la masse et consomment le matériel mucilagineux, puis s’enfouissent dans le sédiment. La phase larvaire se décompose en 4 phases distinctes (Environnement Canada, 1997), séparés par une mue :

- les larves du 1er stade (durée 4 - 7 jours) sont couleur crème,

- durant le 2nd stade larvaire (durée 4 - 7 jours), la larve initie la production d’hémoglobine et devient rose,

- au 3ème stade (durée 4 - 7 jours), les larves prennent une couleur rouge vif typique,

- au 4ème stade, les larves (durée 4 - 7 jours) ont un corps rouge vif alors que la tête est brun jaunâtre et les ocelles noirs. C’est à la fin de ce stade que la larve mue en nymphe.

Les nymphes de Chironomidae quittent ensuite le sédiment pour atteindre la surface de l’eau, où le processus d’émergence est rapide (quelques minutes). L’émergence des imagos est bimodale, les mâles se développant plus vite que les femelles (Pascoe D. et al., 1989). Les adultes vivent quelques jours pendant lesquels ils cherchent à se reproduire et se disperser.

 

 

Caenorhabditis elegans WWW Server

3 Septembre 2009,

Publié par JMB

Caenorhabditis elegans is a small (about 1 mm long) soil nematode found in temperate regions. In the 1960's Sydney Brenner began using it to study the genetics of development and neurobiology. Since then the community of C elegans researchers has expanded several thousands. See Mark Blaxter's introduction to Caenorhabditis elegans for more information.

On-line C. elegans Resources: here


fluorescent GFP crawling C. elegans worm
Fluorescent worms crawling

from The Morimoto lab

The Earthworm Research Group

31 Août 2009,

Publié par JMB

"The Earthworm Research Group (ERG) is based in the School of Built and Natural Environment at the University of Central Lancashire, in Preston, UK. The ERG has existed as an entity for five years or so, but members of the group have been engaged in this area of research for more than twenty years. We regard ourselves as one of the focal points in this area and welcome contact with respect to collaborative research or simply to answer earthworm-related questions.

The ERG was founded by Drs Kevin Butt and Chris Lowe and has worldwide members and associates.

Research

The last 25 years has seen an enormous expansion in earthworm research with the development of potential profit-related applications in vermiculture and organic waste processing. More recently applied research has investigated the role of earthworms in land restoration, eco-toxicology and environmental monitoring. Major advances have therefore been made in the area of earthworm research but despite this, many fundamental questions still remain unanswered. There is still scope to undertake investigations into a group of organisms which have profound effects on soils.

The ERG has worked extensively with earthworm species from across Britain and from numerous northern temperate regions. Research has concentrated on the practical application of earthworms in areas such as soil restoration, organic waste management, bio-monitoring and eco-toxicology. Current overseas projects are linked with Finland, Ireland, Italy, Poland, Spain and the USA."

Sharleen SPITERI: Stop i don't love you anymore

LE DÉVELOPPEMENT ET LA MORT DES CELLULES

6 Mars 2009,

Publié par JMB

Source : Les années lumières
Journaliste: Pauline Vanasse

LE NOBEL DE MÉDECINE 2002 :
LE DÉVELOPPEMENT ET LA MORT DES CELLULES

Sidney Brenner
John Sulston
Robert Horvitz

Les Britanniques Sydney Brenner et John Sulston ainsi que l'Américain Robert Horvitz ont reçu conjointement en 2002 le prix Nobel de médecine pour leurs découvertes sur la régulation génétique du développement des organes et de la mort programmée des cellules.

Des multitudes de cellules se forment constamment dans notre organisme. En parallèle, des cellules meurent. Cette mort programmée est la clé du développement normal de l'organisme.

Les lauréats ont utilisé le ver nématode Caenorhabditis elegans pour suivre la division des cellules et leur différenciation, de l'œuf fécondé à l'adulte.

Au cours de leurs recherches, les scientifiques ont identifié les gènes qui régissent le développement et la mort programmée des cellules.

Ces découvertes sont d'une grande importance pour la recherche médicale.

Elles ont notamment permis de mieux comprendre les origines d'un bon nombre de maladies.


Pauline Vanasse
nous parle des 3 lauréats et de leurs travaux. Elle a interviewé Siegfried Hekimi, chercheur en génétique moléculaire de l'Université McGill à Montréal : lien

 

Quand génétique rime avec longévité

6 Mars 2009,

Publié par JMB

Source : Radio-Canada
Mise à jour le samedi 26 octobre 2002, 20 h 47 .
.
 
.
Des chercheurs de l'Université de Californie à San Francisco (UCSF) ont réussi à doubler la longévité d'un petit ver de terre par une modification génétique, tout en évitant les effets indésirables habituels qui affectent les capacités de reproduction. La technique utilisée consiste à modifier certains gènes qui régularisent l'activité hormonale, communs à de nombreuses espèces, dont l'humain.

La méthode, expérimentée avec un ver Caenorhabditis elegans d'un millimètre de long, a permis de désactiver un groupe de gènes (daf-2 et daf-16) à différentes étapes de vie de l'animal, pour étudier leurs effets sur la longévité.

D'autres travaux avaient démontré que la désactivation partielle du gène daf-2 permettait de doubler la longévité du ver. Le gène encode un récepteur d'insuline ainsi qu'une hormone facteur de croissance. Ce gène affecte également la reproduction. Mais la nouvelle recherche montre que le gène agit de différentes façons à différents stades de la vie pour contrôler la reproduction ou la longévité, ce qui a permis aux scientifiques de découpler ces deux fonctions.

 
.
Un ver très populaire qui fait la «Une» de la revue Science.
.
Si le gène daf-2 est désactivé juste après la naissance, les vers vivent deux fois plus longtemps mais se reproduisent mal. Par contre, si ce gène peut fonctionner normalement jusqu'au début de l'âge adulte, puis est désactivé, les vers ont une vie prolongée tout en se reproduisant normalement. Le ver Caenorhabditis elegans était déjà connu pour ses records de longévité et, plus récemment, pour avoir partagé la vedette avec les trois chercheurs récompensés par le prix Nobel de médecine 2002. Ce nématode est en effet un modèle de laboratoire hors pair pour l'étude des gènes et des mécanismes cellulaires. Cette étude est publiée dans la revue américaine Science.

The Chironomus Newsletter

3 Mars 2009,

Publié par JMB

The CHIRONOMUS Newsletter on Chironomidae Research (ISSN 0172-1941) is devoted to all aspects of chironomid research and aims to be an updated news bulletin for the Chironomidae research community. The newsletter is published yearly in October, is open access, and can be downloaded free from this website. Research articles for the CHIRONOMUS Newsletter are subject to peer review. The newsletter also contains a current bibliography that is maintained by Odwin Hoffrichter, please send complete references of your new Chironomidae publications to him. Submission deadline for contributions to the newsletter is July 1.

GENETIC STUDIES OF AGING AND LONGEVITY IN MODEL ORGANISMS

20 Février 2009,

Publié par JMB

GENETIC STUDIES OF AGING AND LONGEVITY IN MODEL ORGANISMS


By Ji Yuan

(August 2004) Original article : link


Aging can be characterized as:
(1) an inevitable consequence of being a multicellular organism;
(2) associated with a random, passive decline in function;
(3) leading to a global loss of homeostasis (the state of sustained equilibrium in which all cells, and all life forms, exist) over time; and
(4) mortality increasing with age [1].
Age is not a disease, but it does predispose an organism to a variety of diseases [2], in the case of humans, this includes heart disease, arthritis, osteoporosis, diabetes, cancer and Alzheimer’s.

Achieving longevity is thought to be caused by a combination of factors. Possessing longevity-enabling genes, lacking disease-predisposing genetic variations and appropriate health-related behavior are all thought to contribute to long life [3] . Therefore, understanding of the genetics of aging and longevity should lead to the discovery of genes and ultimately drugs that slow down the aging process and facilitate people’s ability to delay and perhaps escape age-associated diseases.

Humans’ relatively long life expectancy makes them less attractive as subjects for longevity research. Using short-lived organisms to discover life-span-altering genes is much more feasible. This paper describes the current state of aging and longevity research with model organisms.


Genetic Model Systems

The major genetic model systems used in aging research are those of the filamentous fungus Podospora anserine, baker’s yeast Saccharomyces cerevisiae, the roundworm Canenorhabditis elegans (C. elegans), the fruit fly Drosophila melanogaster (D. melanogaster), and the common mouse.

These model systems have many advantages for genetic dissection of aging and longevity mechanisms. They are small, easy to maintain, and have a short life span. For instance, life cycle of yeasts and worms is only few days. This allows experiments to be concluded within weeks of their initiation. In addition, there is significant homology between the human genome and those of simpler organisms. About one-fifth of human disease genes that have been positionally cloned possess yeast homologues, reflecting a remarkable degree of genetic conservation [4].

Several genetic methodologies have been used to study aging in these organisms [2]. Mutagenesis is a method that affects the expression of genes or the structure of gene products by altering of DNA sequences using physical or chemical treatment, followed by screening for individuals that possess the resultant phenotypes (visible characteristics and/or behavior that result from the interaction of an organism’s genotype and the environment). Molecular genetics strategies are similar except that they target known genetic loci that are thought to be involved in expressing the phenotype of interest. Quantitative trait loci (QTL) analysis encompasses a family of techniques that are used to zero in on the location of genes responsible for the variation in a particular phenotype. Selective breeding is used to progressively comb together the genetic variants in a population that are responsible for a particular trait by choosing individuals with the most extreme phenotypic expression for breeding. These genetic methodologies have now identified 35 cloned genes that determine longevity in model organisms. These genes encode a wide variety of proteins with a variety of functions, but they can be categorized into four broad physiological processes that play a role in aging: metabolic control, resistance to stress, gene dysregulation, and genetic stability. Insulin is the major hormone controlling critical energy functions. Below is an example of an insulin-like signaling pathway that plays a role in the control of metabolism, development and longevity in C. elegans.


Insulin-like signaling pathway

Studies of long-lived mutants of the nematode C. elegans have contributed significantly to the progress made in the study of aging during the last decade. An example of what has been learned is the discovery of an insulin-like signaling pathway that regulates longevity and metabolism in C. elegans [5].

 

insulinlikepath[2]-1.gif
Figure 1: An insulin-like signaling pathway may regulate longevity in C. elegans. High concentration of insulin-like ligands activate AGE-1 and PDK-1, which activate AKT-1 and AKT-2. These enzymes negatively regulate expression of DAF-16, which is involved in dauer arrest.

 


After embryonic development and hatching, the worms move through a series of four larval stages (L1-L4) before reaching adulthood. If they encounter particular environmental stress, worms will enter the dauer larval stage, which allows worms to survive adverse conditions. When favourable environmental conditions arise, dauer larvae resume development and proceed to L4 larval stage and subsequently to adulthood (Figure 2). In dauer state, worms can survive up to 6 months, which is much longer than adult worm life span (2-3 weeks). The increase in lifespan of the dauer state is not entirely due to reduced metabolism, but also due to increased levels of antioxidant enzyme and stress-resistance proteins [6]. The insulin-like pathway is part of a global endocrine system that controls whether the worms grow reproductively or arrest at the dauer stage.

During the time of dauer formation, numerous dauer formation (daf) genes are active and some of them play roles in determining the two alternative developmental fates (dauer or L3 stage) of C. elegans. These regulatory genes were identified by two general classes of mutants: dauer defective and dauer constitutive mutants. Mutants that possess Dauer constitutive genes such as daf-2 and age-1 which constitute components of the C. elegans insulin signaling pathway live 2 to 3 times longer than wild type [8-10]. Conversely, daf-16 dauer defective mutants suppress the increase in longevity caused by daf-2 and age-1 mutants. Based on previous genetic studies, several dauer genes have been ordered into an insulin-like signaling pathway [5,11-15]. Under reproductive growth conditions, high daf-2 receptor signaling activates age-1 and pdk-1 which in turn, activates the akt-1 and -2 kinases, which negatively regulate daf-16 activity. Inactivated daf-16 fails to further activate the genes necessary for dauer arrest and long life span or repress the genes that inhibit reproductive growth and short life span [7]. Under dauer inducing conditions, these kinase cascades are inactive, so then active daf-16 represses genes required for reproductive growth and short life span, and/or activate genes necessary for dauer arrest and long life span [7]. (Figure 1)

 

wormcycle.gif

Figure 2. The life cycle of C. elegans can be interupted by the dauer stage if environmental conditions are not favourable.

 


In addition to metabolism, the C. elegans insulin pathway regulates free radical protection [16]. Moreover, the insulin pathway in worm aging may be related to the longevity increase caused by caloric restriction in mammals [17]. Caloric restriction in mammals may cause a decline in insulin-like signaling that induces a partial diapause state [18], like that induced in weak daf-2 and age-1 mutants.

Recently, two research group described mutants of genes that modulate pathways homologous to insulin signaling pathways in humans and increase life span of D. melanogaster. A mutation of the insulin-like receptor gene [19], which is homologous to the C. elegans daf-2 gene, and a mutation of the D. melanogaster gene chico 20, which participates in an insulin-like signaling pathway, are associated with a significant increase in life span. Thus, the role of insulin-like signaling pathways appears to be evolutionarily conserved in a number of species, suggesting the importance of investigating such pathways and their relation to aging and longevity in humans.


Conclusion

Genetic studies in simpler organisms demonstrate that specific genes have potent influences on life span. These findings provide a framework for understanding the factors by which life span is determined in lower organisms. More importantly, organism models provide interesting phenotypic characteristics and candidate pathways to be studied in relation to longevity, such as parameters of metabolic control, stress resistance and genetic instability. However, investigation of human homologues of these genes would naturally be more complicated because aging and susceptibility to diseases associated with aging in human is influenced by multiple genes as well as environment factors.


Glossary

1. Mutagenesis - The production of either random or specific mutations in a piece of cloned DNA. Typically, the DNA will then be reintroduced into a cell or an organism to assess the results of the mutagenesis.

2. Quantitative Trait Loci - Continuous traits are often measured and given a quantitative value. Therefore, they are often referred to as quantitative traits, and the area of genetics that studies their mode of inheritance is called quantitative genetics. Many human phenotypes such as IQ, learning ability and blood pressure are quantitative traits. These traits are controlled by multiple genes, each segregating according to Mendel’s laws.

3. Metabolic Control - Mechanisms by which the chemical reactions that occur in a living cell are controlled.


References

1. Helfand, S.L. & Rogina, B. Molecular genetics of aging in the fly: is this the end of the beginning? Bioessays 25, 134-41 (2003).

2. Jazwinski, S.M. Aging and longevity genes. Acta Biochim Pol 47, 269-79 (2000).

3.Perls, T., Kunkel, L. & Puca, A. The genetics of aging. Curr Opin Genet Dev 12, 362-9 (2002).

4. Bassett, D.E., Jr. et al. Genome cross-referencing and XREFdb: implications for the identification and analysis of genes mutated in human disease. Nat Genet 15, 339-44 (1997).

5. Kimura, K.D., Tissenbaum, H.A., Liu, Y. & Ruvkun, G. daf-2, an insulin receptor-like gene that regulates longevity and diapause in Caenorhabditis elegans. Science 277, 942-6 (1997).

6.Murakami, S. & Johnson, T.E. A genetic pathway conferring life extension and resistance to UV stress in Caenorhabditis elegans. Genetics 143, 1207-18 (1996).

7. Finch, C.E. & Ruvkun, G. The genetics of aging. Annu Rev Genomics Hum Genet 2, 435-62 (2001).

8. Dorman, J.B., Albinder, B., Shroyer, T. & Kenyon, C. The age-1 and daf-2 genes function in a common pathway to control the lifespan of Caenorhabditis elegans. Genetics 141, 1399-406 (1995).

9. Kenyon, C., Chang, J., Gensch, E., Rudner, A. & Tabtiang, R. A C. elegans mutant that lives twice as long as wild type. Nature 366, 461-4 (1993).

10. Larsen, P.L., Albert, P.S. & Riddle, D.L. Genes that regulate both development and longevity in Caenorhabditis elegans. Genetics 139, 1567-83 (1995).A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans. Nature 382, 536-9 (1996).

11. Morris, J.Z., Tissenbaum, H.A. & Ruvkun, G.

12. Ogg, S. et al. The Fork head transcription factor DAF-16 transduces insulin-like metabolic and longevity signals in C. elegans. Nature 389, 994-9 (1997).

13. Ogg, S. & Ruvkun, G. The C. elegans PTEN homolog, DAF-18, acts in the insulin receptor-like metabolic signaling pathway. Mol Cell 2, 887-93 (1998).

14. Paradis, S. & Ruvkun, G. Caenorhabditis elegans Akt/PKB transduces insulin receptor-like signals from AGE-1 PI3 kinase to the DAF-16 transcription factor. Genes Dev 12, 2488-98 (1998).

15. Paradis, S., Ailion, M., Toker, A., Thomas, J.H. & Ruvkun, G. A PDK1 homolog is necessary and sufficient to transduce AGE-1 PI3 kinase signals that regulate diapause in Caenorhabditis elegans. Genes Dev 13, 1438-52 (1999).

16. Taub, J. et al. A cytosolic catalase is needed to extend adult lifespan in C. elegans daf-C and clk-1 mutants. Nature 399, 162-6 (1999).

17. Sohal, R.S. & Weindruch, R. Oxidative stress, caloric restriction, and aging. Science 273, 59-63 (1996).

18. Tauber MJ, T.C., Masaki S. Seasonal Adaptation of Insects., 411pp. (Oxford Univ. Press, New York, 1986).

19. Tatar, M. et al. A mutant Drosophila insulin receptor homolog that extends life-span and impairs neuroendocrine function. Science 292, 107-10 (2001).

20. Clancy, D.J. et al. Extension of life-span by loss of CHICO, a Drosophila insulin receptor substrate protein. Science 292, 104-6 (2001).

(Art by Jen Philpot)

WormBook : The Online Review of C.elegans Biology

20 Février 2009,

Publié par JMB

WormBook is a comprehensive, open-access collection of original, peer-reviewed chapters covering topics related to the biology of Caenorhabditis elegans (C. elegans). WormBook also includes WormMethods, an up-to-date collection of methods and protocols for C. elegans researchers.