News 1
Après les analyses phénotypiques extra-ordinaires, mais connues depuis longtemps, de l’ornithorynque, l’analyse de son génome apporte des éclaircissements fascinants.
Notamment, les gènes codant pour ses protéines de lait sont très proches de ceux des autres mammifères ; alors que les gènes codant pour le venin des mâles, est très proches de ceux des reptiles.
Avis personnel : l’éloignement géographique de l’océanie, et donc l’absence quasi-totale de prédateurs naturels fait de ce continent un TRESOR biologique.
Cf. comment Darwin a eu ses premières idées…
Abstract sur le sujet, paru dans Nature cette semaine.
Nature. 2008 May 8;453(7192):175-183
Genome analysis of the platypus reveals unique signatures of evolution.
Warren WC, Hillier LW, Marshall Graves JA, Birney E, Ponting CP, Grützner F, Belov K, Miller W, Clarke L, Chinwalla AT, Yang SP, Heger A, Locke DP, Miethke et al.
Genome Sequencing Center, Washington University School of Medicine, Campus Box 8501, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA.
We present a draft genome sequence of the platypus, Ornithorhynchus anatinus. This monotreme exhibits a fascinating combination of reptilian and mammalian characters. For example, platypuses have a coat of fur adapted to an aquatic lifestyle; platypus females lactate, yet lay eggs; and males are equipped with venom similar to that of reptiles. Analysis of the first monotreme genome aligned these features with genetic innovations. We find that reptile and platypus venom proteins have been co-opted independently from the same gene families; milk protein genes are conserved despite platypuses laying eggs; and immune gene family expansions are directly related to platypus biology. Expansions of protein, non-protein-coding RNA and microRNA families, as well as repeat elements, are identified. Sequencing of this genome now provides a valuable resource for deep mammalian comparative analyses, as well as for monotreme biology and conservation.
News 2
Une étude publiée dans l’un des trois principaux journaux de médecine au monde (le JAMA), confirme avec des data très solides que chez les femmes :
-Fumer augmente de près de 300% le risque de décès
-Plus on commence tôt, plus le risque est élevé.
-Arrêter, permet de diminuer rapidement certains risques
-Après 20, le sur-risque disparait.
Abstract ci-dessous
JAMA. 2008 May 7;299(17):2037-47.Click here to read Links
Smoking and smoking cessation in relation to mortality in women.
Kenfield SA, Stampfer MJ, Rosner BA, Colditz GA.
Department of Epidemiology, Harvard School of Public Health, and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. skenfiel@hsph.harvard.edu
CONTEXT: Smoking is associated with an increased risk of total and cause-specific death, but the rate of mortality risk reduction after quitting compared with continuing to smoke is uncertain. There is inadequate or insufficient evidence to infer the presence or absence of a causal relationship between smoking and ovarian cancer and colorectal cancer. OBJECTIVE: To assess the relationship between cigarette smoking and smoking cessation on total and cause-specific mortality in women. DESIGN, SETTING, AND PARTICIPANTS: Prospective observational study of 104,519 female participants in the Nurses' Health Study with follow-up from 1980 to 2004. MAIN OUTCOME MEASURE: Hazard ratios (HRs) for total mortality, further categorized into vascular and respiratory diseases, lung cancer, other cancers, and other causes. RESULTS: A total of 12,483 deaths occurred in this cohort, 4485 (35.9%) among never smokers, 3602 (28.9%) among current smokers, and 4396 (35.2%) among past smokers. Compared with never smokers, current smokers had an increased risk of total mortality (HR, 2.81; 95% confidence interval [CI], 2.68-2.95) and all major cause-specific mortality. The HR for cancers classified by the 2004 surgeon general's report to be smoking-related was 7.25 (95% CI, 6.43-8.18) and 1.58 (95% CI, 1.45-1.73) for other cancers. Compared with never smokers, the HR for colorectal cancer was 1.63 (95% CI, 1.29-2.05) for current smokers and 1.23 (95% CI, 1.02-1.49) for former smokers. A significant association was not observed for ovarian cancer. Significant trends were observed for earlier age at initiation of smoking for total mortality (P = .003), respiratory disease mortality (P = .001), and all smoking-related cancer mortality (P = .001). The excess risk for all-cause mortality decreases to the level of a never smoker 20 years after quitting, with different time frames for risk reduction observed across outcomes. Approximately 64% of deaths among current smokers and 28% of deaths among former smokers were attributable to cigarette smoking. CONCLUSIONS: Most of the excess risk of vascular mortality due to smoking in women may be eliminated rapidly upon cessation and within 20 years for lung diseases. Postponing the age of smoking initiation reduces the risk of respiratory disease, lung cancer, and other smoking-related cancer deaths but has little effect on other cause-specific mortality. These data suggest that smoking is associated with an increased risk of colorectal cancer mortality but not ovarian cancer mortality.
News 3
Vous pensiez tous que le coq et la poule domestiques (Gallus Gallus domestica) étaient la descendance directe du Coq Doré (Gallus Gallus). N’est-ce pas ?
D’ailleurs je viens de vérifier, même Wikipédia l’affirme (ahaha).
Ben non, notre bon poulet fermier est en fait la descendance hybride du Coq Doré ET du Coq de Sonnerat (Gallus sonneratii).
Plus sérieusement, c’est qui m’intéresse dans cette affaire, c’est que ce « grand » mystère a été décortiqué grâce à l’analyse génétique rigoureuse de l’origine…de la couleur jaune de la peau de nos poules au pot sur pattes.
Abstract ci-dessous de Plos génétique, un des journaux scientifiques les plus prestigieux qui soit.
Il n’y a pas à dire, j’adore mon métier…
PLoS Genet. 2008 Feb 29;4(2):e1000010.Click here to read Click here to read Links
Identification of the yellow skin gene reveals a hybrid origin of the domestic chicken.
Eriksson J, Larson G, Gunnarsson U, Bed'hom B, Tixier-Boichard M, Strömstedt L, Wright D, Jungerius A, Vereijken A, Randi E, Jensen P, Andersson L.
Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden.
Yellow skin is an abundant phenotype among domestic chickens and is caused by a recessive allele (W*Y) that allows deposition of yellow carotenoids in the skin. Here we show that yellow skin is caused by one or more cis-acting and tissue-specific regulatory mutation(s) that inhibit expression of BCDO2 (beta-carotene dioxygenase 2) in skin. Our data imply that carotenoids are taken up from the circulation in both genotypes but are degraded by BCDO2 in skin from animals carrying the white skin allele (W*W). Surprisingly, our results demonstrate that yellow skin does not originate from the red junglefowl (Gallus gallus), the presumed sole wild ancestor of the domestic chicken, but most likely from the closely related grey junglefowl (Gallus sonneratii). This is the first conclusive evidence for a hybrid origin of the domestic chicken, and it has important implications for our views of the domestication process.