scholarly journals Genome-wide association study reveals putative role of gga-miR-15a in controlling feed conversion ratio in layer chickens

BMC Genomics ◽  
2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Jingwei Yuan ◽  
Sirui Chen ◽  
Fengying Shi ◽  
Guiqin Wu ◽  
Aiqiao Liu ◽  
...  
2020 ◽  
Author(s):  
yuanxin miao ◽  
quanshun mei ◽  
chuanke fu ◽  
mingxing liao ◽  
xinyun Li ◽  
...  

Abstract Background: Feed conversion ratio (FCR) is an important productive trait that largely affects profits in pig industry. Elucidating the genetic mechanisms underpinning the FCR potentially promote the efficiencies of improving FCR through artificial selection. In this study, we integrated a genome-wide association study (GWAS) with transcriptome analyses in different tissues in Yorkshire pigs (YY), aimed at identifying key genes and signaling pathways significantly associated with FCR.Results: A total of 61 significant single nucleotide polymorphism (SNPs) were detected by GWAS in YY. All of these SNPs are located on porcine chromosome (SSC) 5 and the covered region was considered as a quantitative trait locus (QTL) region for FCR. Some genes that distributed around these significant SNPs were considered as the candidates for regulating FCR, including TPH2, FAR2, IRAK3, YARS2, GRIP1, FRS2, CNOT2 and TRHDE. According to the transcriptome analyses in hypothalamus, TPH2 exhibits abilities of regulating the intestinal motility by a serotonergic synapse and an oxytocin signaling pathway. In addition, GRIP1 is involved in a glutamatergic and GABAergic signaling pathway, which regulates FCR through affecting the appetite in pigs. Moreover, GRIP1, FRS2, CNOT2, TRHDE regulates the metabolism in various tissues by a thyroid hormone signaling pathway.Conclusions: Synthesizes results from GWAS and transcriptome analyses, TPH2, GRIP1, FRS2, TRHDE, CNOT2 genes were considered as candidate genes for regulating FCR in Yorkshire pigs. These findings help to improve the understandings of the genetic mechanism of FCR and potentially optimize the design of breeding schemes.


2013 ◽  
Vol 133 (4) ◽  
pp. 929-935 ◽  
Author(s):  
Sigrid Le Clerc ◽  
Lieng Taing ◽  
Khaled Ezzedine ◽  
Julie Latreille ◽  
Olivier Delaneau ◽  
...  

2016 ◽  
Vol 68 (4) ◽  
pp. 932-943 ◽  
Author(s):  
Marta E. Alarcón-Riquelme ◽  
Julie T. Ziegler ◽  
Julio Molineros ◽  
Timothy D. Howard ◽  
Andrés Moreno-Estrada ◽  
...  

2014 ◽  
Vol 131 (3) ◽  
pp. 173-182 ◽  
Author(s):  
A. Wolc ◽  
J. Arango ◽  
T. Jankowski ◽  
I. Dunn ◽  
P. Settar ◽  
...  

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Jeremy Manry ◽  
Quentin B. Vincent ◽  
Christian Johnson ◽  
Maya Chrabieh ◽  
Lazaro Lorenzo ◽  
...  

PLoS Genetics ◽  
2020 ◽  
Vol 16 (10) ◽  
pp. e1009065
Author(s):  
Marco Galardini ◽  
Olivier Clermont ◽  
Alexandra Baron ◽  
Bede Busby ◽  
Sara Dion ◽  
...  

2018 ◽  
Author(s):  
Sodbo Zh. Sharapov ◽  
Yakov A. Tsepilov ◽  
Lucija Klaric ◽  
Massimo Mangino ◽  
Gaurav Thareja ◽  
...  

AbstractGlycosylation is a common post-translational modification of proteins. It is known, that glycans are directly involved in the pathophysiology of every major disease. Defining genetic factors altering glycosylation may provide a basis for novel approaches to diagnostic and pharmaceutical applications. Here, we report a genome-wide association study of the human blood plasma N-glycome composition in up to 3811 people. We discovered and replicated twelve loci. This allowed us to demonstrate a clear overlap in genetic control between total plasma and IgG glycosylation. Majority of loci contained genes that encode enzymes directly involved in glycosylation (FUT3/FUT6, FUT8, B3GAT1, ST6GAL1, B4GALT1, ST3GAL4, MGAT3, and MGAT5). We, however, also found loci that are likely to reflect other, more complex, aspects of plasma glycosylation process. Functional genomic annotation suggested the role of DERL3, which potentially highlights the role of glycoprotein degradation pathway, and such transcription factor as IKZF1.


2017 ◽  
Vol 55 (3) ◽  
pp. 181-188 ◽  
Author(s):  
Lai Fun Thean ◽  
Yee Syuen Low ◽  
Michelle Lo ◽  
Yik-Ying Teo ◽  
Woon-Puay Koh ◽  
...  

BackgroundMultiple single nucleotide polymorphisms (SNPs) have been associated with colorectal cancer (CRC) risk. The role of structural or copy number variants (CNV) in CRC, however, remained unclear. We investigated the role of CNVs in patients with sporadic CRC.MethodsA genome-wide association study (GWAS) was performed on 1000 Singapore Chinese patients aged 50 years or more with no family history of CRC and 1000 ethnicity-matched, age-matched and gender-matched healthy controls using the Affymetrix SNP 6 platform. After 16 principal component corrections, univariate and multivariate segmentations followed by association testing were performed on 1830 samples that passed quality assurance tests.ResultsA rare CNV region (CNVR) at chromosome 14q11 (OR=1.92 (95% CI 1.59 to 2.32), p=2.7e-12) encompassing CHD8, and common CNVR at chromosomes 3q13.12 (OR=1.54 (95% CI 1.33 to 1.77), p=2.9e-9) and 12p12.3 (OR=1.69 (95% CI 1.41 to 2.01), p=2.8e-9) encompassing CD47 and RERG/ARHGDIB, respectively, were significantly associated with CRC risk. CNV loci were validated in an independent replication panel using an optimised copy number assay. Whole-genome expression data in matched tumours of a subset of cases demonstrated that copy number loss at CHD8 was significantly associated with dysregulation of several genes that perturb the Wnt, TP53 and inflammatory pathways.ConclusionsA rare CNVR at 14q11 encompassing the chromatin modifier CHD8 was significantly associated with sporadic CRC risk. Copy number loss at CHD8 altered expressions of genes implicated in colorectal tumourigenesis.


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