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Bentley DR Deloukas P Dunham A French L Gregory SG Humphray SJ Mungall AJ Ross MT Carter NP Dunham I Scott CE Ashcroft KJ Atkinson AL Aubin K Beare DM Bethel G Brady N Brook JC Burford DC Burrill WD Burrows C Butler AP Carder C Catanese JJ Clee CM Clegg SM Cobley V Coffey AJ Cole CG Collins JE Conquer JS Cooper RA Culley KM Dawson E Dearden FL Durbin RM de Jong PJ Dhami PD Earthrowl ME Edwards CA Evans RS Gillson CJ Ghori J Green L Gwilliam R Halls KS Hammond S Harper GL Heathcott RW Holden JL 《Nature》2001,409(6822):942-943
We constructed maps for eight chromosomes (1, 6, 9, 10, 13, 20, X and (previously) 22), representing one-third of the genome, by building landmark maps, isolating bacterial clones and assembling contigs. By this approach, we could establish the long-range organization of the maps early in the project, and all contig extension, gap closure and problem-solving was simplified by containment within local regions. The maps currently represent more than 94% of the euchromatic (gene-containing) regions of these chromosomes in 176 contigs, and contain 96% of the chromosome-specific markers in the human gene map. By measuring the remaining gaps, we can assess chromosome length and coverage in sequenced clones. 相似文献
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Most of the world's cod (Gadus morhua) fisheries are now tightly regulated or closed altogether. Being able to link individual fish to their population of origin would assist enormously in policing regulations and in identifying poachers. Here we show that microsatellite genetic markers can be used to assign individual cod from three different populations in the northeastern Atlantic Ocean to their population of origin. 相似文献
949.
Zaugg CE Spaniol M Kaufmann P Bellahcene M Barbosa V Tolnay M Buser PT Krähenbühl S 《Cellular and molecular life sciences : CMLS》2003,60(4):767-775
Carnitine is essential for mitochondrial metabolism of long-chain fatty acids and thus for myocardial energy production. Accordingly, carnitine deficiency can be associated with cardiomyopathy. To better understand this disease, we determined myocardial function and energy metabolism in a rat model of carnitine deficiency. Carnitine deficiency was induced by a 3- or 6-week diet containing N-trimethyl-hydrazine-3-propionate, reducing cardiac and plasma carnitine by 70-85%. Myocardial function was investigated in isolated isovolumic heart preparations. Carnitine-deficient hearts showed left ventricular systolic dysfunction, reduced contractile reserve, and a blunted frequency-force relationship independently of the substrate used (glucose or palmitate). After glycogen depletion, palmitate could not sustain myocardial function. Histology and activities of carnitine palmitoyl transferase, citrate synthase, and cytochrome c oxidase were unaltered. Thus, as little as 3-6 weeks of systemic carnitine deficiency can lead to abnormalities in myocardial function. These abnormalities are masked by endogenous glycogen and are not accompanied by structural alterations of the myocardium or by altered activities of important mitochondrial enzymes. 相似文献
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Averna M De Tullio R Capini P Salamino F Pontremoli S Melloni E 《Cellular and molecular life sciences : CMLS》2003,60(12):2669-2678
The amount of calpastatin directly available in cytosol is under the control of [Ca2+] and [cyclic AMP]. Prolonged calpain activation also promotes degradation of calpastatin. The fluctuation of calpastatin concentration in cell soluble fraction is accompanied by an initial decrease in calpastatin gene expression, followed by a fivefold increase in its expression when the inhibitor protein is degraded. This process can be conceptualized as a mechanism to regulate calpastatin availability in the cell. This conclusion is supported by the fact that calpain, the other component of this proteolytic system, undergoes changes in its levels of expression in a much more limited manner. Furthermore, this process can be observed both in cells exposed to different natural stimuli, or in other cell lines. Modification of calpastatin gene expression might represent a new tool for the in vivo control of the regulatory machinery required for the modulation of Ca2+-dependent proteolysis.Received 18 July 2003; received after revision 3 September 2003; accepted 23 September 2003 相似文献