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231.
Tenhola-Roininen T Kalendar R Schulman AH Tanhuanpää P 《Journal of applied genetics》2011,52(3):299-304
A rye doubled haploid (DH) mapping population (Amilo × Voima) segregating for pre-harvest sprouting (PHS) was generated through
anther culture of F1 plants. A linkage map was constructed using DHs, to our knowledge, for the first time in rye. The map was composed of 289
loci: amplified fragment length polymorphism (AFLP), microsatellite, random amplified polymorphic DNA (RAPD), retrotransposon-microsatellite
amplified polymorphism (REMAP), inter-retrotransposon amplified polymorphism (IRAP), inter-simple sequence repeat (ISSR) and
sequence-related amplified polymorphism (SRAP) markers, and extended altogether 732 cM (one locus in every 2.5 cM). All of
the seven rye chromosomes and four unplaced groups were formed. Distorted segregation of markers (P ≤ 0.05) was detected on all chromosomes. One major quantitative trait locus (QTL) affecting α-amylase activity was found,
which explained 16.1% of phenotypic variation. The QTL was localized on the long arm of chromosome 5R. Microsatellites SCM74,
RMS1115, and SCM77, nearest to the QTL, can be used for marker-assisted selection as a part of a rye breeding program to decrease
sprouting damage. 相似文献
232.
Sanjiv Kumar Peter E. Oishi Ruslan Rafikov Saurabh Aggarwal Yali Hou Sanjeev A. Datar Shruti Sharma Anthony Azakie Jeffrey R. Fineman Stephen M. Black PhD 《Journal of cellular biochemistry》2013,114(2):435-447
We have previously shown that acute increases in pulmonary blood flow (PBF) are limited by a compensatory increase in pulmonary vascular resistance (PVR) via an endothelin‐1 (ET‐1) dependent decrease in nitric oxide synthase (NOS) activity. The mechanisms underlying the reduction in NO signaling are unresolved. Thus, the purpose of this study was to elucidate mechanisms of this ET‐1–NO interaction. Pulmonary arterial endothelial cells were acutely exposed to shear stress in the presence or absence of tezosentan, a combined ETA/ETB receptor antagonist. Shear increased NOx, eNOS phospho‐Ser1177, and H2O2 and decreased catalase activity; tezosentan enhanced, while ET‐1 attenuated all of these changes. In addition, ET‐1 increased eNOS phospho‐Thr495 levels. In lambs, 4 h of increased PBF decreased H2O2, eNOS phospho‐Ser1177, and NOX levels, and increased eNOS phospho‐Thr495, phospho‐catalase, and catalase activity. These changes were reversed by tezosentan. PEG‐catalase reversed the positive effects of tezosentan on NO signaling. In all groups, opening the shunt resulted in a rapid increase in PBF by 30 min. In vehicle‐ and tezosentan/PEG‐catalase lambs, PBF did not change further over the 4 h study period. PVR fell by 30 min in vehicle‐ and tezosentan‐treated lambs, and by 60 min in tezosentan/PEG‐catalase‐treated lambs. In vehicle‐ and tezosentan/PEG‐catalase lambs, PVR did not change further over the 4 h study period. In tezosentan‐treated lambs, PBF continued to increase and LPVR to decrease over the 4 h study period. We conclude that acute increases in PBF are limited by an ET‐1 dependent decrease in NO production via alterations in catalase activity, H2O2 levels, and eNOS phosphorylation. J. Cell. Biochem. 114: 435–447, 2013. © 2012 Wiley Periodicals, Inc. 相似文献
233.
Jelger A. Lycklama a Nijeholt Ruslan Vietrov Gea K. Schuurman-Wolters Bert Poolman 《Journal of molecular biology》2018,430(6):853-866
Solute transport via ATP binding cassette (ABC) importers involves receptor-mediated substrate binding, which is followed by ATP-driven translocation of the substrate across the membrane. How these steps are exactly initiated and coupled, and how much ATP it takes to complete a full transport cycle, are subject of debate. Here, we reconstitute the ABC importer GlnPQ in nanodiscs and in proteoliposomes and determine substrate-(in)dependent ATP hydrolysis and transmembrane transport. We determined the conformational states of the substrate-binding domains (SBDs) by single-molecule Förster resonance energy transfer measurements. We find that the basal ATPase activity (ATP hydrolysis in the absence of substrate) is mainly caused by the docking of the closed-unliganded state of the SBDs onto the transporter domain of GlnPQ and that, unlike glutamine, arginine binds both SBDs but does not trigger their closing. Furthermore, comparison of the ATPase activity in nanodiscs with glutamine transport in proteoliposomes shows that the stoichiometry of ATP per substrate is close to two. These findings help understand the mechanism of transport and the energy coupling efficiency in ABC transporters with covalently linked SBDs, which may aid our understanding of Type I ABC importers in general. 相似文献
234.
Olga Rafikova Mary L. Meadows Jason M. Kinchen Robert P. Mohney Emin Maltepe Ankit A. Desai Jason X.-J. Yuan Joe G. N. Garcia Jeffrey R. Fineman Ruslan Rafikov Stephen M. Black 《PloS one》2016,11(3)
There is increasing interest in the potential for metabolic profiling to evaluate the progression of pulmonary hypertension (PH). However, a detailed analysis of the metabolic changes in lungs at the early stage of PH, characterized by increased pulmonary artery pressure but prior to the development of right ventricle hypertrophy and failure, is lacking in a preclinical animal model of PH. Thus, we undertook a study using rats 14 days after exposure to monocrotaline (MCT), to determine whether we could identify early stage metabolic changes prior to the manifestation of developed PH. We observed changes in multiple pathways associated with the development of PH, including activated glycolysis, increased markers of proliferation, disruptions in carnitine homeostasis, increased inflammatory and fibrosis biomarkers, and a reduction in glutathione biosynthesis. Further, our global metabolic profile data compare favorably with prior work carried out in humans with PH. We conclude that despite the MCT-model not recapitulating all the structural changes associated with humans with advanced PH, including endothelial cell proliferation and the formation of plexiform lesions, it is very similar at a metabolic level. Thus, we suggest that despite its limitations it can still serve as a useful preclinical model for the study of PH. 相似文献
235.
An underground burst of diversity – a new look at the phylogeny and taxonomy of the genus Talpa Linnaeus, 1758 (Mammalia: Talpidae) as revealed by nuclear and mitochondrial genes
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Anna A. Bannikova Elena D. Zemlemerova Paolo Colangelo Mustafa Sözen M. Sevindik Artem A. Kidov Ruslan I. Dzuev Boris Kryštufek Vladimir S. Lebedev 《Zoological Journal of the Linnean Society》2015,175(4):930-948
Using both nuclear and mitochondrial sequences, we demonstrate high genetic differentiation in the genus Talpa and confirm the existence of cryptic species in the Caucasus and Anatolia, namely, T. talyschensis Vereschagin, 1945, T. ognevi Stroganov, 1948, and Talpa ex gr. levantis. Our data support four clades in the genus Talpa that showed strong geographical associations. The ‘europaea’ group includes six species from the western portion of the genus' range (T. europaea, T. occidentalis, T. romana, T. caeca, T. stankovici, and T. levantis s.l.); another three groups are distributed further east: the ‘caucasica’ group (Caucasus), the ‘davidiana’ group (eastern Anatolia and Elburz) and T. altaica (Siberia). The phylogenetic position of T. davidiana was highlighted for the first time. The order of basal branching remains controversial, which can be attributed to rapid diversification events. The molecular time estimates based on nuclear concatenation estimated the basal divergence of the crown Talpa during the latest Miocene. A putative scenario of Talpa radiation and issues of species delimitation are discussed. © 2015 The Linnean Society of London 相似文献
236.
Ruslan Strogantsev Felix Krueger Kazuki Yamazawa Hui Shi Poppy Gould Megan Goldman-Roberts Kirsten McEwen Bowen Sun Roger Pedersen Anne C. Ferguson-Smith 《Genome biology》2015,16(1)
BackgroundSelective maintenance of genomic epigenetic imprints during pre-implantation development is required for parental origin-specific expression of imprinted genes. The Kruppel-like zinc finger protein ZFP57 acts as a factor necessary for maintaining the DNA methylation memory at multiple imprinting control regions in early mouse embryos and embryonic stem (ES) cells. Maternal-zygotic deletion of ZFP57 in mice presents a highly penetrant phenotype with no animals surviving to birth. Additionally, several cases of human transient neonatal diabetes are associated with somatic mutations in the ZFP57 coding sequence.ResultsHere, we comprehensively map sequence-specific ZFP57 binding sites in an allele-specific manner using hybrid ES cell lines from reciprocal crosses between C57BL/6J and Cast/EiJ mice, assigning allele specificity to approximately two-thirds of all binding sites. While half of these are biallelic and include endogenous retrovirus (ERV) targets, the rest show monoallelic binding based either on parental origin or on genetic background of the allele. Parental-origin allele-specific binding is methylation-dependent and maps only to imprinting control differentially methylated regions (DMRs) established in the germline. We identify a novel imprinted gene, Fkbp6, which has a critical function in mouse male germ cell development. Genetic background-specific sequence differences also influence ZFP57 binding, as genetic variation that disrupts the consensus binding motif and its methylation is often associated with monoallelic expression of neighboring genes.ConclusionsThe work described here uncovers further roles for ZFP57-mediated regulation of genomic imprinting and identifies a novel mechanism for genetically determined monoallelic gene expression.
Electronic supplementary material
The online version of this article (doi:10.1186/s13059-015-0672-7) contains supplementary material, which is available to authorized users. 相似文献237.
238.
Dundar Ayca Bayramov Ruslan Onal Muge G. Akkus Mustafa Dogan Muhammet E. Kenanoglu Sercan Cerrah Gunes Meltem Kazimli Ulviye Ozbek Mehmet N. Ercan Oya Yildirim Ruken Celmeli Gamze Parlak Mesut Dundar Ismail Hatipoglu Nihal Unluhizarci Kursad Akalin Hilal Ozkul Yusuf Saatci Cetin Dundar Munis 《Molecular biology reports》2019,46(4):3677-3690
Molecular Biology Reports - Congenital adrenal hyperplasia (CAH) is an autosomal recessive genetic disorder due to presence of mutations in the genes involved in the metabolism of steroid hormones... 相似文献
239.
Ruth Simmons Ruslan Malyuta Nelli Chentsova Antonia Medoeva Yuri Kruglov Alexander Yurchenko Andrew Copas Kholoud Porter CASCADE Collaboration in EuroCoord 《PloS one》2015,10(8)