Articles importants dans Nature, Science ou Cell

[MaliciaR]

Vu que notre pubmed-crawleuse préférée est sur la touche ...

Ah bon? Inadmissible


Bon, voici un truc franchement marrant même si c'est un peu abrupt :


Implementing Arithmetic and Other Analytic Operations By Transcriptional Regulation


Sean M. Cory1, Theodore J. Perkins2, PLoS Computational Biology

1 Department of Human Genetics, McGill University, Montreal, Quebec, Canada
2 School of Computer Science, McGill University, McGill Centre for Bioinformatics, Montreal, Quebec, Canada

The transcriptional regulatory machinery of a gene can be viewed as a computational device, with transcription factor concentrations as inputs and expression level as the output. This view begs the question: what kinds of computations are possible? We show that different parameterizations of a simple chemical kinetic model of transcriptional regulation are able to approximate all four standard arithmetic operations: addition, subtraction, multiplication, and division, as well as various equality and inequality operations. This contrasts with other studies that emphasize logical or digital notions of computation in biological networks. We analyze the accuracy and precision of these approximations, showing that they depend on different sets of parameters, and are thus independently tunable. We demonstrate that networks of these “arithmetic” genes can be combined to accomplish yet more complicated computations by designing and simulating a network that detects statistically significant elevations in a time-varying signal. We also consider the much more general problem of approximating analytic functions, showing that this can be achieved by allowing multiple transcription factor binding sites on the promoter. These observations are important for the interpretation of naturally occurring networks and imply new possibilities for the design of synthetic networks.


Le reste de l'article est ici (en open acces ) : http://www.ploscompbiol.org/article/...l.pcbi.1000064

Bonne lecture


Cordialement,
-----

[jmbowie]

Un aspect de l'évolution bactérienne. Très intéressant, mais je n'ai pas encore lu l'article. A bientôt


BMC Evol Biol. 2008 Jan 28;8:31.

The origin of a novel gene through overprinting in Escherichia coli.


BACKGROUND: Overlapped genes originate by a) loss of a stop codon among
contiguous genes coded in different frames; b) shift to an upstream initiation
codon of one of the contiguous genes; or c) by overprinting, whereby a novel open
reading frame originates through point mutation inside an existing gene. Although
overlapped genes are common in viruses, it is not clear whether overprinting has
led to new genes in prokaryotes. RESULTS: Here we report the origin of a new gene
through overprinting in Escherichia coli K12. The htgA gene coding for a positive
regulator of the sigma 32 heat shock promoter arose by point mutation in a
123/213 phase within an open reading frame (yaaW) of unknown function, most
likely in the lineage leading to E. coli and Shigella sp. Further, we show that
yaaW sequences coding for htgA genes have a slower evolutionary rate than those
lacking an overlapped htgA gene. CONCLUSION: While overprinting has been shown to
be rather frequent in the evolution of new genes in viruses, our results suggest
that this mechanism has also contributed to the origin of a novel gene in a
prokaryote. We propose the term janolog (from Jano, the two-faced Roman god) to
describe the homology relationship that holds between two genes when one
originated through overprinting of the other. One cannot dismiss the possibility
that at least a small fraction of the large number of novel ORPhan genes detected
in pan-genome and metagenomic studies arose by overprinting.

[Vinc]

La découverte des loci de l'autisme, cette semaine dans Science

Identifying Autism Loci and Genes by Tracing Recent Shared Ancestry

Eric M. Morrow,1,2,3,4,5* Seung-Yun Yoo,1,2,4,5* Steven W. Flavell,5,6 Tae-Kyung Kim,5,6 Yingxi Lin,5,6 Robert Sean Hill,1,2,4,5 Nahit M. Mukaddes,7 Soher Balkhy,8 Generoso Gascon,8,9 Asif Hashmi,10 Samira Al-Saad,11 Janice Ware,5,12 Robert M. Joseph,5,13 Rachel Greenblatt,1,2 Danielle Gleason,1,2 Julia A. Ertelt,1,2 Kira A. Apse,1,2,5 Adria Bodell,1,2 Jennifer N. Partlow,1,2 Brenda Barry,1,2 Hui Yao,1 Kyriacos Markianos,1 Russell J. Ferland,14 Michael E. Greenberg,5,6 Christopher A. Walsh1,2,4,5

To find inherited causes of autism-spectrum disorders, we studied families in which parents share ancestors, enhancing the role of inherited factors. We mapped several loci, some containing large, inherited, homozygous deletions that are likely mutations. The largest deletions implicated genes, including PCDH10 (protocadherin 10) and DIA1 (deleted in autism1, or c3orf58), whose level of expression changes in response to neuronal activity, a marker of genes involved in synaptic changes that underlie learning. A subset of genes, including NHE9 (Na+/H+ exchanger 9), showed additional potential mutations in patients with unrelated parents. Our findings highlight the utility of "homozygosity mapping" in heterogeneous disorders like autism but also suggest that defective regulation of gene expression after neural activity may be a mechanism common to seemingly diverse autism mutations.


Science 11 July 2008:
Vol. 321. no. 5886, pp. 218 - 223
DOI: 10.1126/science.1157657



V.

[MaliciaR]

Hello,

Voilà une revue dans Nature, je l'ai relue 2 fois de suite tellement elle est intéressante!

Nature Reviews Molecular Cell Biology 9, 569-574 (July 2008) | doi:10.1038/nrm2426

Opinion: Extra-chromosomal elements and the evolution of cellular DNA replication machineries
Adam T. McGeoch & Stephen D. Bell

DNA replication is fundamental to the propagation of cellular life. Remarkably, the bacterial replication machinery is distinct from that used by archaea and eukaryotes. In this article, we discuss the role that lateral gene transfer by extra-chromosomal elements might have had in shaping the replication machinery and even modulating the manner in which host cellular genomes are replicated.


La suite est là : http://www.nature.com/nrm/journal/v9...l/nrm2426.html

Bonne lecture


Cordialement,

[MaliciaR]

Bonjour,

Une autre revue, excellente aussi Sortie pour le numéro du mois d'Août de Nature


Nature Reviews Genetics 9, 605-618 (August 2008) | doi:10.1038/nrg2386

Horizontal gene transfer in eukaryotic evolution
Patrick J. Keeling1 & Jeffrey D. Palmer2


Horizontal gene transfer (HGT; also known as lateral gene transfer) has had an important role in eukaryotic genome evolution, but its importance is often overshadowed by the greater prevalence and our more advanced understanding of gene transfer in prokaryotes. Recurrent endosymbioses and the generally poor sampling of most nuclear genes from diverse lineages have also complicated the search for transferred genes. Nevertheless, the number of well-supported cases of transfer from both prokaryotes and eukaryotes, many with significant functional implications, is now expanding rapidly. Major recent trends include the important role of HGT in adaptation to certain specialized niches and the highly variable impact of HGT in different lineages.


Bonne lecture


Cordialement,

[Vinc]

Protease-catalysed protein splicing: a new post-translational modification?

Ivana Saska and David J. Craik
Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD 4072, Australia

In all organisms, proteases catalyse peptide-bond
hydrolysis and mediate protein function for a multitude
of cellular processes. Mechanistically, nothing prevents
proteases from also catalysing peptide-bond ligation;
however, this ‘reverse’ reaction rarely is observed. In
eukaryotes its presence has been viewed as an anomaly.
Recent studies from plants and animals now challenge
this assumption, indicating that protease-catalysed
protein splicing is a bona fide post-translational modification.
Increasing evidence indicates that the proximity
of protein substrates, imposed either by their structure
or by the physical constraints of the local environment,
dictates when the splicing reaction will occur. This previously
under-recognized splicing mechanism could
increase intracellular protein diversity, thereby expanding
the size of the proteome and sequence diversity
beyond the predictions from genomic studies.

Trends in Biochemical Sciences Vol.33 No.8, 2008


V.

[mantOs]

Personne ne parle du virophage, qui bouleverse pourtant le monde de la virologie.

Le premier virus qui infecte les virus.


The virophage as a unique parasite of the giant mimivirus.

Nature. 2008 Sep 4

La Scola B, Desnues C, Pagnier I, Robert C, Barrassi L, Fournous G, Merchat M, Suzan-Monti M, Forterre P, Koonin E, Raoult D.

Viruses are obligate parasites of Eukarya, Archaea and Bacteria. Acanthamoeba polyphaga mimivirus (APMV) is the largest known virus; it grows only in amoeba and is visible under the optical microscope. Mimivirus possesses a 1,185-kilobase double-stranded linear chromosome whose coding capacity is greater than that of numerous bacteria and archaea1, 2, 3. Here we describe an icosahedral small virus, Sputnik, 50 nm in size, found associated with a new strain of APMV. Sputnik cannot multiply in Acanthamoeba castellanii but grows rapidly, after an eclipse phase, in the giant virus factory found in amoebae co-infected with APMV4. Sputnik growth is deleterious to APMV and results in the production of abortive forms and abnormal capsid assembly of the host virus. The Sputnik genome is an 18.343-kilobase circular double-stranded DNA and contains genes that are linked to viruses infecting each of the three domains of life Eukarya, Archaea and Bacteria. Of the 21 predicted protein-coding genes, eight encode proteins with detectable homologues, including three proteins apparently derived from APMV, a homologue of an archaeal virus integrase, a predicted primase-helicase, a packaging ATPase with homologues in bacteriophages and eukaryotic viruses, a distant homologue of bacterial insertion sequence transposase DNA-binding subunit, and a Zn-ribbon protein. The closest homologues of the last four of these proteins were detected in the Global Ocean Survey environmental data set5, suggesting that Sputnik represents a currently unknown family of viruses. Considering its functional analogy with bacteriophages, we classify this virus as a virophage. The virophage could be a vehicle mediating lateral gene transfer between giant viruses.

[invite74366261]

Personne ne parle du virophage, qui bouleverse pourtant le monde de la virologie.

Le premier virus qui infecte les virus.

A propos du virophage, quelqu'un aurait une réponse pour Benjamin qui se demande quelle différence il y a avec les virus satellites ?

[invite43dd87ea]

Après les travaux de Yamanaka, Jaenish et consort voilà ce qui vient de sortir... On s'approche de plus en plus d'un vrai traitement contre certaine maladie incurable !!

Induced Pluripotent Stem Cells Generated Without Viral Integration.

Stadtfeld M, Nagaya M, Utikal J, Weir G, Hochedlinger K.

Science. 2008 Sep 25.

Pluripotent stem cells have been generated from mouse and human somatic cells by viral expression of the transcription factors Oct4, Sox2, Klf4, and c-Myc. A major limitation of this technology is the use of potentially harmful genome-integrating viruses. Here, we generate mouse induced pluripotent stem cells (iPS) from fibroblasts and liver cells by using nonintegrating adenoviruses transiently expressing Oct4, Sox2, Klf4, and c-Myc. These adenoviral iPS (adeno-iPS) cells show DNA demethylation characteristic of reprogrammed cells, express endogenous pluripotency genes, form teratomas, and contribute to multiple tissues, including the germ line, in chimeric mice. Our results provide strong evidence that insertional mutagenesis is not required for in vitro reprogramming. Adenoviral reprogramming may provide an improved method for generating and studying patient-specific stem cells and for comparing embryonic stem cells and iPS cells.

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

[piwi]

C'est vrai que la stratégie est intéressante même si le rendement est encore assez faible. Je pense aussi que nous sommes sur la voie d'une révolution douce. Sans effusion de spectaculaire les progrès sont réguliers. On entre dans des contraintes techniques mais on a quand même l'impression que les verrous sautent le plus naturellement du monde les uns après les autres.

[pimd]

Et voila une nouvelle hormone végétale (et je le cite pas juste parce que c'est mon equipe !) responsable du contrôle de l'architecture des plantes supérieures !

Strigolactone inhibition of shoot branching.

Nature. 2008 Sep 11;455(7210):189-94.Click here to read

Gomez-Roldan V, Fermas S, Brewer PB, Puech-Pagès V, Dun EA, Pillot JP, Letisse F, Matusova R, Danoun S, Portais JC, Bouwmeester H, Bécard G, Beveridge CA, Rameau C, Rochange SF.

[invite43dd87ea]

Toujours dans le domaine de la reprogrammation cellulaire :
Sauf que là c'est IN VIVO !!

In vivo reprogramming of adult pancreatic exocrine cells to beta-cells.

Zhou Q, Brown J, Kanarek A, Rajagopal J, Melton DA.

Department of Stem Cell and Regenerative Biology, Howard Hughes Medical Institute, Harvard Stem Cell Institute, Harvard University, 7 Divinity Avenue, Cambridge, Massachusetts 02138, USA.

One goal of regenerative medicine is to instructively convert adult cells into other cell types for tissue repair and regeneration. Although isolated examples of adult cell reprogramming are known, there is no general understanding of how to turn one cell type into another in a controlled manner. Here, using a strategy of re-expressing key developmental regulators in vivo, we identify a specific combination of three transcription factors (Ngn3 (also known as Neurog3) Pdx1 and Mafa) that reprograms differentiated pancreatic exocrine cells in adult mice into cells that closely resemble beta-cells. The induced beta-cells are indistinguishable from endogenous islet beta-cells in size, shape and ultrastructure. They express genes essential for beta-cell function and can ameliorate hyperglycaemia by remodelling local vasculature and secreting insulin. This study provides an example of cellular reprogramming using defined factors in an adult organ and suggests a general paradigm for directing cell reprogramming without reversion to a pluripotent stem cell state.


http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

[MaliciaR]

Ha là là, je trouve que ça manque cruellement de Procaryotes, ces derniers temps
Voilà une revue toute fraîche :


Nature Reviews Microbiology 6, 805-814 (November 2008) | doi:10.1038/nrmicro1991

Hydrothermal vents and the origin of life

William Martin, John Baross, Deborah Kelley & Michael J. Russell


Submarine hydrothermal vents are geochemically reactive habitats that harbour rich microbial communities. There are striking parallels between the chemistry of the H2–CO2 redox couple that is present in hydrothermal systems and the core energy metabolic reactions of some modern prokaryotic autotrophs. The biochemistry of these autotrophs might, in turn, harbour clues about the kinds of reactions that initiated the chemistry of life. Hydrothermal vents thus unite microbiology and geology to breathe new life into research into one of biology's most important questions — what is the origin of life?

La suite et bonne lecture!

[LXR]

Désolé pour Malicia mais on revient en puissance dans l'eucaryote, le développement embryonnaire plus exactement, conjugaison d'audace et de prouesse technique de la part des auteurs.

Published Online October 9, 2008
Science DOI: 10.1126/science.1162493


Reconstruction of Zebrafish Early Embryonic Development by Scanned Light Sheet Microscopy

Philipp J. Keller 1*, Annette D. Schmidt 2, Joachim Wittbrodt 3*, Ernst H. K. Stelzer 4

A long-standing goal of biology is to map the behavior of all cells during vertebrate embryogenesis. We developed digital scanned laser light sheet fluorescence microscopy and recorded nuclei localization and movement in entire wild-type and mutant zebrafish embryos over the first 24 hours of development. Multiview in vivo imaging at 1.5 billion voxels per minute provides "digital embryos" (i.e., comprehensive databases of cell positions, divisions, and migratory tracks). Our analysis of global cell division patterns reveals a maternally defined initial morphodynamic symmetry break, which identifies the embryonic body axis. We further derive a model of germ layer formation and show that the mesendoderm forms from one-third of the embryo's cells in a single event. Our digital embryos, with 55 million nucleus entries, are provided as a resource.

Lien PubMed

Surtout attardez vous sur les films qui sont assez impressionnants!

Enjoy!

Greg

[Vinc]

Bonjour!

Un papier de psychopathe cette semaine dans Science, par l'équipe de Stephen Elledge.
En très gros, les auteurs ont mis au point une technique (à base de micro-array et de FACS) permettant de cribler les protéines dégradées par le protéasome et comme ils sont joueurs, ils se sont "amusé" à tester cette technique sur une banque de 8000 ORFs...
Très très gros papier.

Global Protein Stability Profiling in Mammalian Cells

Hsueh-Chi Sherry Yen, Qikai Xu,* Danny M. Chou,* Zhenming Zhao, Stephen J. Elledge

The abundance of cellular proteins is determined largely by the rate of transcription and translation coupled with the stability of individual proteins. Although we know a great deal about global transcript abundance, little is known about global protein stability. We present a highly parallel multiplexing strategy to monitor protein turnover on a global scale by coupling flow cytometry with microarray technology to track the stability of individual proteins within a complex mixture. We demonstrated the feasibility of this approach by measuring the stability of 8000 human proteins and identifying proteasome substrates. The technology provides a general platform for proteome-scale analysis of protein turnover under various physiological and disease conditions.

www.sciencemag.org SCIENCE VOL 322 7 NOVEMBER 2008


V.

[Vinc]

Après avoir lu l'article, je dois dire qu'il me laisse sceptique car les auteurs ont utilisés l'EGFP fusionné aux ORFs pour faire leur banque.

Mais il a été montré il y a quelques temps maintenant que l'EGFP inhibe l'ubiquitination des protéines fusionnées.
Cela apporte un biais énorme et je trouve très étrange que quelqu'un de la trempe de Steve Elledge n'ait pas tenu compte de ce facteur.

Nous leur avons écrit en leur signalant ce "détail" et je vous tiendrai au courant dès que nous aurons une réponse (pour ceux que cela intéresse).

V.

[invite43dd87ea]

Petite question j'ai des soucis avec les flux rss des jounaux publiées par CELL, avez vous le même soucis?

[Vinc]

Après avoir lu l'article, je dois dire qu'il me laisse sceptique car les auteurs ont utilisés l'EGFP fusionné aux ORFs pour faire leur banque.

Mais il a été montré il y a quelques temps maintenant que l'EGFP inhibe l'ubiquitination des protéines fusionnées.
Cela apporte un biais énorme et je trouve très étrange que quelqu'un de la trempe de Steve Elledge n'ait pas tenu compte de ce facteur.

Nous leur avons écrit en leur signalant ce "détail" et je vous tiendrai au courant dès que nous aurons une réponse (pour ceux que cela intéresse).

V.

Pour finir sur cette histoire, pour ceux que cela intéresse. Elledge nous a répondu, il n'était pas au courant du papier et nous a fourni une explication bancale. Je ne suis définitivement pas convaincu par ce papier. MP pour plus de détails.

V.

[invite43dd87ea]

Interessant tout ça je suis pas du tout expert de ce domaine, mais c'est quand même fou qu'un papier avec autant de travail, publié dans science, peut être détruit par un seul élément .
En tout cas ça montre bien que les publis sont loin d'être rempli de vérité absolue.

[Vinc]

Disons que non la technique est extrêmement ingénieuse, le travail est énorme et Elledge reste un maitre et un excellent biologiste (encore heureux ).
Mais j'avoue que ce "détail" n'en est en fait pas un et me perturbe pour l'analyse des data... Ajouter à cela des protéines très connues qui sont réellement dégradée par le protéasome (comme p53) et qui sont classées dans le papier comme étant non dégradées. Mais comme toute approche de masse, on a toujours des faux positifs ou négatifs (même si p53 aurait été un bon contrôle positif de la manipe). On peut supposer que les protéines positives (trouvées comme étant dégradées) dans cette étude le sont vraiment, mais la fusion EGFP introduit certainement des faux négatifs et on passe donc à coté d'autres protéines qui sont réellement dégradées mais pas détectées car la GFP inhibe leur poly-ubiquitination K48.

Et oui plus généralement cela rappelle que de nombreux papiers (si ce n'est tous) contiennent des erreurs ou des raccourcis parfois abusifs. Je ne sais plus où j'avais lu (et qui disait) que 90% des publications sont fausses et que seules 10% sont réellement de nouvelles découvertes.
Ce chiffre parait énorme mais malheureusement beaucoup de résultats sont sur-interprétés.

V.

[invite74366261]

Je ne sais plus où j'avais lu (et qui disait) que 90% des publications sont fausses et que seules 10% sont réellement de nouvelles découvertes.

Ça doit être cet article de John Ioannidis de 2005 (accès libre) : http://dx.doi.org/10.1371/journal.pmed.0020124

[doubleD]

Salut à tous

Intéressant papier sur de l'édition par insertion chez l'homme. Pas aussi bien que dans les mitos mais bon....

Curr Biol. 2008 Nov 5. [Epub ahead of print]

Evidence for Insertional RNA Editing in Humans.

Zougman A, Zió?kowski P, Mann M, Wi?niewski JR.

Department of Proteomics and Signal Transduction, Max Planck Institute for Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany; Center for Integrated Protein Science, D-81377 Munich, Germany.

Large-scale analysis directly at the protein level holds the promise of uncovering features not apparent or present at the gene level [1-3]. Although mass spectrometry (MS)-based proteomics can now identify and quantify thousands of cellular proteins in large-scale proteomics experiments, much of the peptide information contained in these experiments remains unassigned [4]. Here, we use such information to discover a previously unreported mechanism creating altered protein forms. Linker histones H1 and high-mobility group (HMG) proteins are abundant nuclear proteins that regulate gene expression through modulation of chromatin structure [5-8]. In the high-resolution MS analysis of histone H1 and HMG protein fractions isolated from human cells, we discovered peptides that mapped upstream of the known translation start sites of these genes. No alternative upstream start site exists in the genome, but analysis of Expressed Sequence Tag (EST) databases revealed that these N-terminally extended (ET) proteins are due to in-frame translation of the 5' untranslated region (5'UTR) sequences of the transcripts. The new translation start sites are created by a single uridine insertion between AG, reflecting a previously unreported RNA-editing mechanism. To our knowledge, this is the first report of RNA-insertion editing in humans and may be an example of the type of discoveries possible with modern proteomics methods.

[LXR]

Salut,

Pas un article mais une petite vidéo libre sur le site de Cell. Ca intéressera surtout les virologistes mais c'est sympa pour les autres aussi.

DNA Packaging by T4 bacteriophage

Greg

[a freind]

Salut tous le monde.
J'ai aimé ce file car il donne des liens de différentes catégories biologiques et j'aimerai bien en faire partie en participant par un lien en biologie cellulaire (des cours en format PDF et vidéo) qui me semble trés éfficace pour faire des études ou mème pour la révision des cours, c'est comme si vous étiez à la faq quoi [http://www.wikinu.org/medecine/index...laire_Grenoble].
Cependant j'ai vu qu'il y a 149 page que j'ai pas pu tous les consulter, alors je ne sais pas si ce lien est déja proposé ou non, mais de toute façon je vais le poster, et je m'excuse si il l'est déja.

[inviteec2476e7]

je viens de decouvrir cette discussion passionnante!
j'aurais juste une remarque a vous faire.
dans certains post, certains proposent seul l'abstract, sans plus de commentaires.
Je ne suis pas chercheur, (et bien décidée a ne pas tremper plus que le bout de l'orteil dans ce monde ..(de brutes)...!) et donc peu habituée a parcourir en diagonale un article en anglais.

Je propose que vous mettiez au moins l'objet de l'article, ou de la "decouverte" en intro de l'abstract... en francais...
ainsi, je parle pour moi, je vois si je m'y penche dessus ou si je passe...

sinon, c'est une tres bonne idée !!

bon courage dans vos labos !

[LXR]

Bonjour,

Un article paru aujourd'hui dans Nature, conduit par Paul Nurse, et qui traite un sujet fondateur de la biologie cellulaire : le lien entre la taille de la cellule et l'entrée en mitose. Les travaux ont été réalisés chez Schizosaccharoyces pombe, modèle classiquement utilisé pour étudier les phénomènes de gradient intracellulaire.

A spatial gradient coordinates cell size and mitotic entry in fission yeast

Many eukaryotic cell types undergo size-dependent cell cycle transitions controlled by the ubiquitous cyclin-dependent kinase Cdk1 (refs 1–4). The proteins that control Cdk1 activity are well described but their links with mechanisms monitoring cell size remain elusive. In the fission yeast Schizosaccharomyces pombe, cells enter mitosis and divide at a defined and reproducible size owing to the regulated activity of Cdk1 (refs 2, 3). Here we show that the cell polarity protein kinase Pom1, which localizes to cell ends5, regulates a signalling network that contributes to the control of mitotic entry. This network is located at cortical nodes in the middle of interphase cells, and these nodes contain the Cdk1 inhibitor Wee1, the Wee1-inhibitory kinases Cdr1 (also known as Nim1) and Cdr2, and the anillin-like protein Mid1. Cdr2 establishes the hierarchical localization of other proteins in the nodes, and receives negative regulatory signals from Pom1. Pom1 forms a polar gradient extending from the cell ends towards the cell middle and acts as a dose-dependent inhibitor of mitotic entry, working through the Cdr2 pathway. As cells elongate, Pom1 levels decrease at the cell middle, leading to mitotic entry. We propose that the Pom1 polar gradient and the medial cortical nodes generate information about cell size and coordinate this with mitotic entry by regulating Cdk1 through Pom1, Cdr2, Cdr1 and Wee1.

Espérons que Mariano Barbacid reprenne le filon chez les cellules de mammifères.

Greg

[jmbowie]

Une brevia dans Science:

The SOS Response Controls Integron Recombination
Émilie Guerin,1,* Guillaume Cambray,2,* Neus Sanchez-Alberola,3,* Susana Campoy,3 Ivan Erill,4 Sandra Da Re,1 Bruno Gonzalez-Zorn,5 Jordi Barbé,3 Marie-Cécile Ploy,1 Didier Mazel2,{dagger}

Integrons are found in the genome of hundreds of environmental bacteria but are mainly known for their role in the capture and spread of antibiotic resistance determinants among Gram-negative pathogens. We report a direct link between this system and the ubiquitous SOS response. We found that LexA controlled expression of most integron integrases and consequently regulated cassette recombination. This regulatory coupling enhanced the potential for cassette swapping and capture in cells under stress, while minimizing cassette rearrangements or loss in constant environments. This finding exposes integrons as integrated adaptive systems and has implications for antibiotic treatment policies.

[Pfhoryan]

Un édito et un article dans Science (Parker et al, Science 2009, vol25, p995) sur la duplication de gène par rétrotransposition de mRNA comme facteur d'évolution.

C'est différent d'une duplication classique de gène car seule la séquence codante étant dupliquée, la régulation de l'expression dépend de la zone d'intégration et peut donc être fortement différente de celle du gène d'origine. L'article décrit une transposition de ce type pour un facteur de croissance de fibroblaste, à l'origine du phénotype "pattes courtes" chez différentes races de chien.

--
"Toute vérité franchit trois étapes. D’abord elle est ridiculisée. Ensuite, elle subit une forte opposition. Puis, elle est considérée comme ayant toujours été une évidence." - Arthur Schopenhauer

[MaliciaR]

Un autre Science très intéressant :

Genetic code supports targeted insertion of two amino acids by one codon

Turanov AA, Lobanov AV, Fomenko DE, Morrison HG, Sogin ML, Klobutcher LA, Hatfield DL, Gladyshev VN; Science. 2009 Jan 9;323(5911):259-61


Strict one-to-one correspondence between codons and amino acids is thought to be an essential feature of the genetic code. However, we report that one codon can code for two different amino acids with the choice of the inserted amino acid determined by a specific 3' untranslated region structure and location of the dual-function codon within the messenger RNA (mRNA). We found that the codon UGA specifies insertion of selenocysteine and cysteine in the ciliate Euplotes crassus, that the dual use of this codon can occur even within the same gene, and that the structural arrangements of Euplotes mRNA preserve location-dependent dual function of UGA when expressed in mammalian cells. Thus, the genetic code supports the use of one codon to code for multiple amino acids.

[LXR]

Décidément en biologie ça ne fait jamais en se simplifiant...

Greg