scholarly journals Peer Review #1 of "Whole-genome single-nucleotide polymorphism (SNP) marker discovery and association analysis with the eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) content in Larimichthys crocea (v0.1)"

2016 ◽  
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Docosahexaenoic Acid ◽  
Eicosapentaenoic Acid ◽  
Peer Review ◽  
Association Analysis ◽  
Whole Genome ◽  
Nucleotide Polymorphism ◽  
Larimichthys Crocea ◽  
Single Nucleotide ◽  
Marker Discovery

scholarly journals Whole-genome single-nucleotide polymorphism (SNP) marker discovery and association analysis with the eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) content inLarimichthys crocea

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2664 ◽  
Author(s):  
Shijun Xiao ◽  
Panpan Wang ◽  
Linsong Dong ◽  
Yaguang Zhang ◽  
Zhaofang Han ◽  
...  
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Docosahexaenoic Acid ◽  
Eicosapentaenoic Acid ◽  
Snp Markers ◽  
Large Yellow Croaker ◽  
Whole Genome ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Commercial Fish ◽  
Snp Development

Whole-genome single-nucleotide polymorphism (SNP) markers are valuable genetic resources for the association and conservation studies. Genome-wide SNP development in many teleost species are still challenging because of the genome complexity and the cost of re-sequencing. Genotyping-By-Sequencing (GBS) provided an efficient reduced representative method to squeeze cost for SNP detection; however, most of recent GBS applications were reported on plant organisms. In this work, we used anEcoRI-NlaIII based GBS protocol to teleost large yellow croaker, an important commercial fish in China and East-Asia, and reported the first whole-genome SNP development for the species. 69,845 high quality SNP markers that evenly distributed along genome were detected in at least 80% of 500 individuals. Nearly 95% randomly selected genotypes were successfully validated by Sequenom MassARRAY assay. The association studies with the muscle eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) content discovered 39 significant SNP markers, contributing as high up to ∼63% genetic variance that explained by all markers. Functional genes that involved in fat digestion and absorption pathway were identified, such asAPOB,CRATandOSBPL10. Notably,PPT2Gene, previously identified in the association study of the plasma n-3 and n-6 polyunsaturated fatty acid level in human, was re-discovered in large yellow croaker. Our study verified thatEcoRI-NlaIII based GBS could produce quality SNP markers in a cost-efficient manner in teleost genome. The developed SNP markers and the EPA and DHA associated SNP loci provided invaluable resources for the population structure, conservation genetics and genomic selection of large yellow croaker and other fish organisms.

scholarly journals Whole-Genome Single-Nucleotide-Polymorphism Analysis for Discrimination of Clostridium botulinum Group I Strains

2014 ◽  
Vol 80 (7) ◽  
pp. 2125-2132 ◽  
Author(s):  
Narjol Gonzalez-Escalona ◽  
Ruth Timme ◽  
Brian H. Raphael ◽  
Donald Zink ◽  
Shashi K. Sharma
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Clostridium Botulinum ◽  
Toxin Gene ◽  
Polymorphism Analysis ◽  
Snp Analysis ◽  
Whole Genome ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Content Type ◽  
Group I

ABSTRACTClostridium botulinumis a genetically diverse Gram-positive bacterium producing extremely potent neurotoxins (botulinum neurotoxins A through G [BoNT/A-G]). The complete genome sequences of three strains harboring only the BoNT/A1 nucleotide sequence are publicly available. Although these strains contain a toxin cluster (HA+OrfX−) associated with hemagglutinin genes, little is known about the genomes of subtype A1 strains (termed HA−OrfX+) that lack hemagglutinin genes in the toxin gene cluster. We sequenced the genomes of three BoNT/A1-producingC. botulinumstrains: two strains with the HA+OrfX−cluster (69A and 32A) and one strain with the HA−OrfX+cluster (CDC297). Whole-genome phylogenic single-nucleotide-polymorphism (SNP) analysis of these strains along with other publicly availableC. botulinumgroup I strains revealed five distinct lineages. Strains 69A and 32A clustered with theC. botulinumtype A1 Hall group, and strain CDC297 clustered with theC. botulinumtype Ba4 strain 657. This study reports the use of whole-genome SNP sequence analysis for discrimination ofC. botulinumgroup I strains and demonstrates the utility of this analysis in quickly differentiatingC. botulinumstrains harboring identical toxin gene subtypes. This analysis further supports previous work showing that strains CDC297 and 657 likely evolved from a common ancestor and independently acquired separate BoNT/A1 toxin gene clusters at distinct genomic locations.

Association analysis of ERAP1 gene single nucleotide polymorphism in susceptibility to ankylosing spondylitis in Iranian population

2018 ◽  
Vol 201 ◽  
pp. 52-58 ◽  
Author(s):  
Farhad Babaie ◽  
Mehrdad Ebrazeh ◽  
Maryam Hemmatzadeh ◽  
Fatemeh Sadat Mohammadi ◽  
Arezoo Gowhari Shabgah ◽  
...  
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Ankylosing Spondylitis ◽  
Association Analysis ◽  
Iranian Population ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Gene Single Nucleotide Polymorphism

Whole-genome single nucleotide polymorphism-based linkage analysis in spondyloarthritis multiplex families reveals a new susceptibility locus in 13q13

2015 ◽  
Vol 75 (7) ◽  
pp. 1380-1385 ◽  
Author(s):  
Félicie Costantino ◽  
Emmanuel Chaplais ◽  
Tifenn Leturcq ◽  
Roula Said-Nahal ◽  
Ariane Leboime ◽  
...  
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Linkage Analysis ◽  
Susceptibility Locus ◽  
Whole Genome ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Multiplex Families

scholarly journals Whole‐Genome Approach Discovers Novel Genetic and Nongenetic Variance Components Modulated by Lifestyle for Cardiovascular Health

2020 ◽  
Vol 9 (8) ◽  
Author(s):  
Xuan Zhou ◽  
Julius van der Werf ◽  
Kristin Carson‐Chahhoud ◽  
Guiyan Ni ◽  
John McGrath ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Body Mass Index ◽  
Heart Rate ◽  
Single Nucleotide Polymorphism ◽  
Cardiovascular Risk ◽  
Lifestyle Factors ◽  
Whole Genome ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Cardiovascular Traits

Background Both genetic and nongenetic factors can predispose individuals to cardiovascular risk. Finding ways to alter these predispositions is important for cardiovascular disease prevention. Methods and Results We used a novel whole‐genome approach to estimate the genetic and nongenetic effects on—and hence their predispositions to—cardiovascular risk and determined whether they vary with respect to lifestyle factors such as physical activity, smoking, alcohol consumption, and dietary intake. We performed analyses on the ARIC (Atherosclerosis Risk in Communities) Study (N=6896–7180) and validated findings using the UKBB (UK Biobank, N=14 076–34 538). Lifestyle modulation was evident for many cardiovascular traits such as body mass index and resting heart rate. For example, alcohol consumption modulated both genetic and nongenetic effects on body mass index, whereas smoking modulated nongenetic effects on heart rate, pulse pressure, and white blood cell count. We also stratified individuals according to estimated genetic and nongenetic effects that are modulated by lifestyle factors and showed distinct phenotype–lifestyle relationships across the stratified groups. Finally, we showed that neglecting lifestyle modulations of cardiovascular traits would on average reduce single nucleotide polymorphism heritability estimates of these traits by a small yet significant amount, primarily owing to the overestimation of residual variance. Conclusions Lifestyle changes are relevant to cardiovascular disease prevention. Individual differences in the genetic and nongenetic effects that are modulated by lifestyle factors, as shown by the stratified group analyses, implies a need for personalized lifestyle interventions. In addition, single nucleotide polymorphism–based heritability of cardiovascular traits without accounting for lifestyle modulations could be underestimated.

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