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341.
We conducted a 4-year experiment to assess the impacts of rotational cattle grazing on rodents and raptors in a mesic coastal grassland in northwestern California. Live-trapping indicated that rodent abundance declined by 69% on the grazed area and increased by 14% on the ungrazed area. Raptor use of the grazed area declined by 15% and increased on the ungrazed area by 63%. Measures of giving-up density indicated that rodents perceived a 25% higher predation risk on grazed area than on ungrazed area, but raptor hunting surveys indicated that risk of depredation from raptors was 2.5 times lower in the grazed habitat, suggesting that rodents use indirect vegetative cues to assess risk. 相似文献
342.
L. Lee Grismer Perry L. Wood Jr Myint Kyaw Thura Thaw Zin Evan S. H. Quah Matthew L. Murdoch 《Journal of Natural History》2018,52(13-16):881-915
ABSTRACTA phylogenetic taxonomy of the gekkonid genus Hemiphyllodactylus based on molecular, morphological, and ecological data recovered 28 species, including three new species from the upland regions of the Shan Plateau in eastern Myanmar. Hemiphyllodactylus linnwayensis sp. nov. is a forest-adapted species that may also be a human commensal and H. montawaensis sp. nov. and H. tonywhitteni sp. nov. are karst forest-adapted species. The discovery of three new species from montane regions in eastern Myanmar extends the distribution of a larger monophyletic group of Hemiphyllodactylus westward to the eastern edge of the Ayeyrawady Basin through a series of semi-contiguous, parallel mountain ranges originating in western China and northern Thailand. The discovery of the karst forest-adapted H. montawaensis sp. nov. and H. tonywhitteni sp. nov. further emphasizes the unrealized herpetological diversity endemic to karst ecosystems and the need for increased field work throughout such habitats in South-East Asia.www.zoobank.org/urn:lsid:zoobank.org:pub:E42FA075-E8E0-4005-98AB-12E8D5F23A07 相似文献
343.
M Krauthammer Y Kong BH Ha P Evans A Bacchiocchi JP McCusker E Cheng MJ Davis G Goh M Choi S Ariyan D Narayan K Dutton-Regester A Capatana EC Holman M Bosenberg M Sznol HM Kluger DE Brash DF Stern MA Materin RS Lo S Mane S Ma KK Kidd NK Hayward RP Lifton J Schlessinger TJ Boggon R Halaban 《Nature genetics》2012,44(9):1006-1014
We characterized the mutational landscape of melanoma, the form of skin cancer with the highest mortality rate, by sequencing the exomes of 147 melanomas. Sun-exposed melanomas had markedly more ultraviolet (UV)-like C>T somatic mutations compared to sun-shielded acral, mucosal and uveal melanomas. Among the newly identified cancer genes was PPP6C, encoding a serine/threonine phosphatase, which harbored mutations that clustered in the active site in 12% of sun-exposed melanomas, exclusively in tumors with mutations in BRAF or NRAS. Notably, we identified a recurrent UV-signature, an activating mutation in RAC1 in 9.2% of sun-exposed melanomas. This activating mutation, the third most frequent in our cohort of sun-exposed melanoma after those of BRAF and NRAS, changes Pro29 to serine (RAC1(P29S)) in the highly conserved switch I domain. Crystal structures, and biochemical and functional studies of RAC1(P29S) showed that the alteration releases the conformational restraint conferred by the conserved proline, causes an increased binding of the protein to downstream effectors, and promotes melanocyte proliferation and migration. These findings raise the possibility that pharmacological inhibition of downstream effectors of RAC1 signaling could be of therapeutic benefit. 相似文献
344.
Ellinor PT Lunetta KL Albert CM Glazer NL Ritchie MD Smith AV Arking DE Müller-Nurasyid M Krijthe BP Lubitz SA Bis JC Chung MK Dörr M Ozaki K Roberts JD Smith JG Pfeufer A Sinner MF Lohman K Ding J Smith NL Smith JD Rienstra M Rice KM Van Wagoner DR Magnani JW Wakili R Clauss S Rotter JI Steinbeck G Launer LJ Davies RW Borkovich M Harris TB Lin H Völker U Völzke H Milan DJ Hofman A Boerwinkle E Chen LY Soliman EZ Voight BF Li G Chakravarti A Kubo M Tedrow UB Rose LM Ridker PM Conen D Tsunoda T 《Nature genetics》2012,44(6):670-675
345.
Linear mixed models have attracted considerable attention recently as a powerful and effective tool for accounting for population stratification and relatedness in genetic association tests. However, existing methods for exact computation of standard test statistics are computationally impractical for even moderate-sized genome-wide association studies. To address this issue, several approximate methods have been proposed. Here, we present an efficient exact method, which we refer to as genome-wide efficient mixed-model association (GEMMA), that makes approximations unnecessary in many contexts. This method is approximately n times faster than the widely used exact method known as efficient mixed-model association (EMMA), where n is the sample size, making exact genome-wide association analysis computationally practical for large numbers of individuals. 相似文献
346.
347.
Graubert TA Shen D Ding L Okeyo-Owuor T Lunn CL Shao J Krysiak K Harris CC Koboldt DC Larson DE McLellan MD Dooling DJ Abbott RM Fulton RS Schmidt H Kalicki-Veizer J O'Laughlin M Grillot M Baty J Heath S Frater JL Nasim T Link DC Tomasson MH Westervelt P DiPersio JF Mardis ER Ley TJ Wilson RK Walter MJ 《Nature genetics》2012,44(1):53-57
Myelodysplastic syndromes (MDS) are hematopoietic stem cell disorders that often progress to chemotherapy-resistant secondary acute myeloid leukemia (sAML). We used whole-genome sequencing to perform an unbiased comprehensive screen to discover the somatic mutations in a sample from an individual with sAML and genotyped the loci containing these mutations in the matched MDS sample. Here we show that a missense mutation affecting the serine at codon 34 (Ser34) in U2AF1 was recurrently present in 13 out of 150 (8.7%) subjects with de novo MDS, and we found suggestive evidence of an increased risk of progression to sAML associated with this mutation. U2AF1 is a U2 auxiliary factor protein that recognizes the AG splice acceptor dinucleotide at the 3' end of introns, and the alterations in U2AF1 are located in highly conserved zinc fingers of this protein. Mutant U2AF1 promotes enhanced splicing and exon skipping in reporter assays in vitro. This previously unidentified, recurrent mutation in U2AF1 implicates altered pre-mRNA splicing as a potential mechanism for MDS pathogenesis. 相似文献
348.
349.
Ferreira MA O'Donovan MC Meng YA Jones IR Ruderfer DM Jones L Fan J Kirov G Perlis RH Green EK Smoller JW Grozeva D Stone J Nikolov I Chambert K Hamshere ML Nimgaonkar VL Moskvina V Thase ME Caesar S Sachs GS Franklin J Gordon-Smith K Ardlie KG Gabriel SB Fraser C Blumenstiel B Defelice M Breen G Gill M Morris DW Elkin A Muir WJ McGhee KA Williamson R MacIntyre DJ MacLean AW St CD Robinson M Van Beck M Pereira AC Kandaswamy R McQuillin A Collier DA Bass NJ Young AH Lawrence J Ferrier IN 《Nature genetics》2008,40(9):1056-1058
To identify susceptibility loci for bipolar disorder, we tested 1.8 million variants in 4,387 cases and 6,209 controls and identified a region of strong association (rs10994336, P = 9.1 x 10(-9)) in ANK3 (ankyrin G). We also found further support for the previously reported CACNA1C (alpha 1C subunit of the L-type voltage-gated calcium channel; combined P = 7.0 x 10(-8), rs1006737). Our results suggest that ion channelopathies may be involved in the pathogenesis of bipolar disorder. 相似文献
350.
Bilguvar K Yasuno K Niemelä M Ruigrok YM von Und Zu Fraunberg M van Duijn CM van den Berg LH Mane S Mason CE Choi M Gaál E Bayri Y Kolb L Arlier Z Ravuri S Ronkainen A Tajima A Laakso A Hata A Kasuya H Koivisto T Rinne J Ohman J Breteler MM Wijmenga C State MW Rinkel GJ Hernesniemi J Jääskeläinen JE Palotie A Inoue I Lifton RP Günel M 《Nature genetics》2008,40(12):1472-1477
Stroke is the world's third leading cause of death. One cause of stroke, intracranial aneurysm, affects approximately 2% of the population and accounts for 500,000 hemorrhagic strokes annually in mid-life (median age 50), most often resulting in death or severe neurological impairment. The pathogenesis of intracranial aneurysm is unknown, and because catastrophic hemorrhage is commonly the first sign of disease, early identification is essential. We carried out a multistage genome-wide association study (GWAS) of Finnish, Dutch and Japanese cohorts including over 2,100 intracranial aneurysm cases and 8,000 controls. Genome-wide genotyping of the European cohorts and replication studies in the Japanese cohort identified common SNPs on chromosomes 2q, 8q and 9p that show significant association with intracranial aneurysm with odds ratios 1.24-1.36. The loci on 2q and 8q are new, whereas the 9p locus was previously found to be associated with arterial diseases, including intracranial aneurysm. Associated SNPs on 8q likely act via SOX17, which is required for formation and maintenance of endothelial cells, suggesting a role in development and repair of the vasculature; CDKN2A at 9p may have a similar role. These findings have implications for the pathophysiology, diagnosis and therapy of intracranial aneurysm. 相似文献