Association analysis of transcripts from the bipolar susceptibility locus on chromosome 4q35, exclusion of a pathogenic role for eight positional candidate genes

Author(s):  
Ian P. Blair ◽  
Renee F. Badenhop ◽  
Anna Scimone ◽  
Melissa J. Moses ◽  
Nicholas P. Kerr ◽  
...  
2002 ◽  
Vol 12 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Clyde Francks ◽  
Simon E. Fisher ◽  
Richard K. Olson ◽  
Bruce F. Pennington ◽  
Shelley D. Smith ◽  
...  

2013 ◽  
Vol 93 (3) ◽  
pp. 295-306 ◽  
Author(s):  
B. K. Karisa ◽  
J. Thomson ◽  
Z. Wang ◽  
H. L. Bruce ◽  
G. S. Plastow ◽  
...  

Karisa, B. K., Thomson, J., Wang, Z., Bruce, H. L., Plastow, G. S. and Moore, S. S. 2013. Candidate genes and biological pathways associated with carcass quality traits in beef cattle. Can. J. Anim. Sci. 93: 295–306. The objective of this study was to use the candidate gene approach to identify the genes associated with carcass quality traits in beef cattle steers at the University of Alberta Ranch at Kinsella, Canada. This approach involved identifying positional candidate genes and prioritizing them according to their functions into functional candidate genes before performing statistical association analysis. The positional candidate genes and single nucleotide polymorphisms (SNP) were identified from previously reported quantitative trait loci for component traits including body weight, average daily gain, metabolic weight, feed efficiency and energy balance. Positional candidate genes were then prioritized into functional candidate genes according to the associated gene ontology terms and their functions. A total of 116 genes were considered functional candidate genes and 117 functional SNPs were genotyped and used for multiple marker association analysis using ASReml®. Seven SNPs were significantly associated with various carcass quality traits (P≤0.005). The significant genes were associated with biological processes such as fat, glucose, protein and steroid metabolism, growth, energy utilization and DNA transcription and translation as inferred from the protein knowledgebase (UniprotKB). Gene network analysis indicated significant involvement of biological processes related to fat and steroid metabolism and regulation of transcription and translation of DNA.


BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Gehendra Bhattarai ◽  
Wei Yang ◽  
Ainong Shi ◽  
Chunda Feng ◽  
Braham Dhillon ◽  
...  

Abstract Background Downy mildew, the most devastating disease of spinach (Spinacia oleracea L.), is caused by the oomycete Peronospora effusa [=P. farinosa f. sp. spinaciae]. The P. effusa shows race specificities to the resistant host and comprises 19 reported races and many novel isolates. Sixteen new P. effusa races were identified during the past three decades, and the new pathogen races are continually overcoming the genetic resistances used in commercial cultivars. A spinach breeding population derived from the cross between cultivars Whale and Lazio was inoculated with P. effusa race 16 in an environment-controlled facility; disease response was recorded and genotyped using genotyping by sequencing (GBS). The main objective of this study was to identify resistance-associated single nucleotide polymorphism (SNP) markers from the cultivar Whale against the P. effusa race 16. Results Association analysis conducted using GBS markers identified six significant SNPs (S3_658,306, S3_692697, S3_1050601, S3_1227787, S3_1227802, S3_1231197). The downy mildew resistance locus from cultivar Whale was mapped to a 0.57 Mb region on chromosome 3, including four disease resistance candidate genes (Spo12736, Spo12784, Spo12908, and Spo12821) within 2.69–11.28 Kb of the peak SNP. Conclusions Genomewide association analysis approach was used to map the P. effusa race 16 resistance loci and identify associated SNP markers and the candidate genes. The results from this study could be valuable in understanding the genetic basis of downy mildew resistance, and the SNP marker will be useful in spinach breeding to select resistant lines.


Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 718
Author(s):  
Bingxin Meng ◽  
Tao Wang ◽  
Yi Luo ◽  
Deze Xu ◽  
Lanzhi Li ◽  
...  

Lodging reduces rice yield, but increasing lodging resistance (LR) usually limits yield potential. Stem strength and leaf type are major traits related to LR and yield, respectively. Hence, understanding the genetic basis of stem strength and leaf type is of help to reduce lodging and increase yield in LR breeding. Here, we carried out an association analysis to identify quantitative trait locus (QTLs) affecting stem strength-related traits (internode length/IL, stem wall thickness/SWT, stem outer diameter/SOD, and stem inner diameter/SID) and leaf type-associated traits (Flag leaf length/FLL, Flag leaf angle/FLA, Flag leaf width/FLW, leaf-rolling/LFR and SPAD/Soil, and plant analyzer development) using a diverse panel of 550 accessions and evaluated over two years. Genome-wide association study (GWAS) using 4,076,837 high-quality single-nucleotide polymorphisms (SNPs) identified 89 QTLs for the nine traits. Next, through “gene-based association analysis, haplotype analysis, and functional annotation”, the scope was narrowed down step by step. Finally, we identified 21 candidate genes in 9 important QTLs that included four reported genes (TUT1, OsCCC1, CFL1, and ACL-D), and seventeen novel candidate genes. Introgression of alleles, which are beneficial for both stem strength and leaf type, or pyramiding stem strength alleles and leaf type alleles, can be employed for LR breeding. All in all, the experimental data and the identified candidate genes in this study provide a useful reference for the genetic improvement of rice LR.


Biologia ◽  
2008 ◽  
Vol 63 (1) ◽  
Author(s):  
Eva Slabá ◽  
Pavol Joppa ◽  
Ján Šalagovič ◽  
Ružena Tkáčová

AbstractChronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Irreversible airflow limitation, both progressive and associated with an inflammatory response of the lungs to noxious particles or gases, is a hallmark of the disease. Cigarette smoking is the most important environmental risk factor for COPD, nevertheless, only approximately 20–30% of smokers develop symptomatic disease. Epidemiological studies, case-control studies in relatives of patients with COPD, and twin studies suggest that COPD is a genetically complex disease with environmental factors and many involved genes interacting together. Two major strategies have been employed to identify the genes and the polymorphisms that likely contribute to the development of complex diseases: association studies and linkage analyses. Biologically plausible pathogenetic mechanisms are prerequisites to focus the search for genes of known function in association studies. Protease-antiprotease imbalance, generation of oxidative stress, and chronic inflammation are recognized as the principal mechanisms leading to irreversible airflow obstruction and parenchymal destruction in the lung. Therefore, genes which have been implicated in the pathogenesis of COPD are involved in antiproteolysis, antioxidant barrier and metabolism of xenobiotic substances, inflammatory response to cigarette smoke, airway hyperresponsiveness, and pulmonary vascular remodelling. Significant associations with COPD-related phenotypes have been reported for polymorphisms in genes coding for matrix metalloproteinases, microsomal epoxide hydrolase, glutathione-S-transferases, heme oxygenase, tumor necrosis factor, interleukines 1, 8, and 13, vitamin D-binding protein and β-2-adrenergic receptor (ADRB2), whereas adequately powered replication studies failed to confirm most of the previously observed associations. Genome-wide linkage analyses provide us with a novel tool to identify the general locations of COPD susceptibility genes, and should be followed by association analyses of positional candidate genes from COPD pathophysiology, positional candidate genes selected from gene expression studies, or dense single nucleotide polymorphism panels across regions of linkage. Haplotype analyses of genes with multiple polymorphic sites in linkage disequilibrium, such as the ADRB2 gene, provide another promising field that has yet to be explored in patients with COPD. In the present article we review the current knowledge about gene polymorphisms that have been recently linked to the risk of developing COPD and/or may account for variations in the disease course.


Sign in / Sign up

Export Citation Format

Share Document