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151.
Van Driessche N Demsar J Booth EO Hill P Juvan P Zupan B Kuspa A Shaulsky G 《Nature genetics》2005,37(5):471-477
Classical epistasis analysis can determine the order of function of genes in pathways using morphological, biochemical and other phenotypes. It requires knowledge of the pathway's phenotypic output and a variety of experimental expertise and so is unsuitable for genome-scale analysis. Here we used microarray profiles of mutants as phenotypes for epistasis analysis. Considering genes that regulate activity of protein kinase A in Dictyostelium, we identified known and unknown epistatic relationships and reconstructed a genetic network with microarray phenotypes alone. This work shows that microarray data can provide a uniform, quantitative tool for large-scale genetic network analysis. 相似文献
152.
Much of the property damage from natural hazards in the United States is caused by landfalling hurricanes--strong tropical cyclones that reach the coast. For the southeastern Atlantic coast of the US, a statistical method for forecasting the occurrence of landfalling hurricanes for the season ahead has been reported, but the physical mechanisms linking the predictor variables to the frequency of hurricanes remain unclear. Here we present a statistical model that uses July wind anomalies between 1950 and 2003 to predict with significant and useful skill the wind energy of US landfalling hurricanes for the following main hurricane season (August to October). We have identified six regions over North America and over the east Pacific and North Atlantic oceans where July wind anomalies, averaged between heights of 925 and 400 mbar, exhibit a stationary and significant link to the energy of landfalling hurricanes during the subsequent hurricane season. The wind anomalies in these regions are indicative of atmospheric circulation patterns that either favour or hinder evolving hurricanes from reaching US shores. 相似文献
153.
Positron emission tomography after MPTP: observations relating to the cause of Parkinson's disease 总被引:5,自引:0,他引:5
D B Calne J W Langston W R Martin A J Stoessl T J Ruth M J Adam B D Pate M Schulzer 《Nature》1985,317(6034):246-248
The dopa analogue 6-fluorodopa (6-FD) used with positron emission tomography (PET) allows in vivo visualization of dopamine and its metabolites in nigrostriatal nerve endings. We have now found abnormal 6-FD scans in four subjects exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). None had parkinsonism. The results suggest subclinical damage to the nigrostriatal pathway. This is the first direct evidence that dopaminergic impairment can exist without clinical deficits. Here we discuss this finding in the context of the hypothesis that Parkinson's disease may stem from clinically silent damage to the substantia nigra, followed by slow attrition of neurones in this region because of its particular vulnerability to cell loss as a normal consequence of ageing. 相似文献
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155.
Mechanical failure modes leading to cracks or breeches in proton exchange membrane fuel cells are driven by mechanical forces associated with swelling from water uptake and shrinkage from dehumidifi-cation. To determine the magnitude of compressive mechanical stress imposed by water swelling in a proton exchange fuel-cell membrane, the osmotic pressure of water in a perfluorosulfonic acid ionomer (Nafion? N 117) membrane was measured using a hydrostatic piston-cylinder device with an in-situ hydrophilic frit. Experiments indicate that hydrostatic stresses greater than 103.5 MPa are created in a membrane when swollen with water at 23℃ suggesting that pressure from water swelling can distort Nafion N 117-based structures as the osmotic pressure is of the same order of magnitude as the flow stress of Nafion N 117. 相似文献
156.
Stefater JA Lewkowich I Rao S Mariggi G Carpenter AC Burr AR Fan J Ajima R Molkentin JD Williams BO Wills-Karp M Pollard JW Yamaguchi T Ferrara N Gerhardt H Lang RA 《Nature》2011,474(7352):511-515
Myeloid cells are a feature of most tissues. Here we show that during development, retinal myeloid cells (RMCs) produce Wnt ligands to regulate blood vessel branching. In the mouse retina, where angiogenesis occurs postnatally, somatic deletion in RMCs of the Wnt ligand transporter Wntless results in increased angiogenesis in the deeper layers. We also show that mutation of Wnt5a and Wnt11 results in increased angiogenesis and that these ligands elicit RMC responses via a non-canonical Wnt pathway. Using cultured myeloid-like cells and RMC somatic deletion of Flt1, we show that an effector of Wnt-dependent suppression of angiogenesis by RMCs is Flt1, a naturally occurring inhibitor of vascular endothelial growth factor (VEGF). These findings indicate that resident myeloid cells can use a non-canonical, Wnt-Flt1 pathway to suppress angiogenic branching. 相似文献
157.
Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma 总被引:1,自引:0,他引:1
Varela I Tarpey P Raine K Huang D Ong CK Stephens P Davies H Jones D Lin ML Teague J Bignell G Butler A Cho J Dalgliesh GL Galappaththige D Greenman C Hardy C Jia M Latimer C Lau KW Marshall J McLaren S Menzies A Mudie L Stebbings L Largaespada DA Wessels LF Richard S Kahnoski RJ Anema J Tuveson DA Perez-Mancera PA Mustonen V Fischer A Adams DJ Rust A Chan-on W Subimerb C Dykema K Furge K Campbell PJ Teh BT Stratton MR Futreal PA 《Nature》2011,469(7331):539-542
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McDermott-Roe C Ye J Ahmed R Sun XM Serafín A Ware J Bottolo L Muckett P Cañas X Zhang J Rowe GC Buchan R Lu H Braithwaite A Mancini M Hauton D Martí R García-Arumí E Hubner N Jacob H Serikawa T Zidek V Papousek F Kolar F Cardona M Ruiz-Meana M García-Dorado D Comella JX Felkin LE Barton PJ Arany Z Pravenec M Petretto E Sanchis D Cook SA 《Nature》2011,478(7367):114-118
Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood. Unbiased systems genetics approaches in the rat now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-α and PGC1α (which are master regulators of mitochondrial and cardiac function), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy. 相似文献