The relationship between MFN1 copy number variation and growth traits of beef cattle

Gene ◽  
2022 ◽  
Vol 811 ◽  
pp. 146071
Author(s):  
Zhi Yao ◽  
Jiaxiao Li ◽  
Zijing Zhang ◽  
Yanan Chai ◽  
Xian Liu ◽  
...  
Gene ◽  
2019 ◽  
Vol 680 ◽  
pp. 99-104 ◽  
Author(s):  
Jia-Wei Xu ◽  
Li Zheng ◽  
Li-Juan Li ◽  
Yu-fei Yao ◽  
He Hua ◽  
...  

Gene ◽  
2021 ◽  
pp. 146014
Author(s):  
Peng Yang ◽  
Cuicui Cai ◽  
Mengxiao Niu ◽  
Xian Liu ◽  
Hongli Wang ◽  
...  

Gene ◽  
2021 ◽  
pp. 146060
Author(s):  
Xinmiao Li ◽  
Xiaoting Ding ◽  
Lingling Liu ◽  
Peng Yang ◽  
Zhi Yao ◽  
...  

Gene ◽  
2020 ◽  
Vol 753 ◽  
pp. 144799
Author(s):  
Jie Cheng ◽  
Rui Jiang ◽  
Yu Yang ◽  
Xiukai Cao ◽  
Yongzhen Huang ◽  
...  

2020 ◽  
Vol 66 (5) ◽  
pp. 718-726
Author(s):  
Yuwei Liu ◽  
Caren E Smith ◽  
Laurence D Parnell ◽  
Yu-Chi Lee ◽  
Ping An ◽  
...  

Abstract Background Copy number variation (CNV) in the salivary amylase gene (AMY1) modulates salivary α-amylase levels and is associated with postprandial glycemic traits. Whether AMY1-CNV plays a role in age-mediated change in insulin resistance (IR) is uncertain. Methods We measured AMY1-CNV using duplex quantitative real-time polymerase chain reaction in two studies, the Boston Puerto Rican Health Study (BPRHS, n = 749) and the Genetics of Lipid-Lowering Drug and Diet Network study (GOLDN, n = 980), and plasma metabolomic profiles in the BPRHS. We examined the interaction between AMY1-CNV and age by assessing the relationship between age with glycemic traits and type 2 diabetes (T2D) according to high or low copy numbers of the AMY1 gene. Furthermore, we investigated associations between metabolites and interacting effects of AMY1-CNV and age on T2D risk. Results We found positive associations of IR with age among subjects with low AMY1-copy-numbers in both studies. T2D was marginally correlated with age in participants with low AMY1-copy-numbers but not with high AMY1-copy-numbers in the BPRHS. Metabolic pathway enrichment analysis identified the pentose metabolic pathway based on metabolites that were associated with both IR and the interactions between AMY1-CNV and age. Moreover, in older participants, high AMY1-copy-numbers tended to be associated with lower levels of ribonic acid, erythronic acid, and arabinonic acid, all of which were positively associated with IR. Conclusions We found evidence supporting a role of AMY1-CNV in modifying the relationship between age and IR. Individuals with low AMY1-copy-numbers tend to have increased IR with advancing age.


2019 ◽  
Vol 60 (2) ◽  
pp. 199-207 ◽  
Author(s):  
Mei Liu ◽  
Bo Li ◽  
Tao Shi ◽  
Yongzhen Huang ◽  
George E. Liu ◽  
...  

Animals ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 688 ◽  
Author(s):  
Ziting Feng ◽  
Xinyu Li ◽  
Jie Cheng ◽  
Rui Jiang ◽  
Ruolan Huang ◽  
...  

Copy number variation (CNV) is a type of genomic variation with an important effect on animal phenotype. We found that the PIGY gene contains a 3600 bp copy number variation (CNV) region located in chromosome 6 of sheep (Oar_v4.0 36,121,601–36,125,200 bp). This region overlaps with multiple quantitative trait loci related to phenotypes like muscle density and carcass weight. Therefore, in this study, the copy number variation of the PIGY gene was screened in three Chinese sheep breeds, namely, Chaka sheep (CKS, May of 2018, Wulan County, Qinghai Province, China), Hu sheep (HS, May of 2015, Mengjin County, Henan Province, China), and small-tailed Han sheep (STHS, May of 2016, Yongjing, Gansu Province, China). Association analyses were performed on the presence of CNV and sheep body size traits. We used real-time quantitative PCR (qPCR) to detect the CNV for association analysis. According to the results, the loss-type CNV was more common than other types in the three breeds (global average: loss = 61.5%, normal = 17.5%, and gain = 21.0%). The association analysis also showed significant effects of the PIGY gene CNV on body weight, chest circumference, and circumference of the cannon bone of sheep. Sheep with gain-type CNV had better growth traits than those with other types. The results indicate a clear relationship between the PIGY gene CNV and growth traits of sheep, suggesting the use of CNV as a new molecular breeding marker.


2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Xin Shao ◽  
Ning Lv ◽  
Jie Liao ◽  
Jinbo Long ◽  
Rui Xue ◽  
...  

Abstract Background Cancer is a heterogeneous disease with many genetic variations. Lines of evidence have shown copy number variations (CNVs) of certain genes are involved in development and progression of many cancers through the alterations of their gene expression levels on individual or several cancer types. However, it is not quite clear whether the correlation will be a general phenomenon across multiple cancer types. Methods In this study we applied a bioinformatics approach integrating CNV and differential gene expression mathematically across 1025 cell lines and 9159 patient samples to detect their potential relationship. Results Our results showed there is a close correlation between CNV and differential gene expression and the copy number displayed a positive linear influence on gene expression for the majority of genes, indicating that genetic variation generated a direct effect on gene transcriptional level. Another independent dataset is utilized to revalidate the relationship between copy number and expression level. Further analysis show genes with general positive linear influence on gene expression are clustered in certain disease-related pathways, which suggests the involvement of CNV in pathophysiology of diseases. Conclusions This study shows the close correlation between CNV and differential gene expression revealing the qualitative relationship between genetic variation and its downstream effect, especially for oncogenes and tumor suppressor genes. It is of a critical importance to elucidate the relationship between copy number variation and gene expression for prevention, diagnosis and treatment of cancer.


Animals ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 1008 ◽  
Author(s):  
Fei Ge ◽  
Congjun Jia ◽  
Min Chu ◽  
Chunnian Liang ◽  
Ping Yan

Copy number variation (CNV) is currently accepted as a common source of genetic variation. It is reported that CNVs may influence the resistance to disease and complex economic traits, such as residual feed intake, muscle formation, and fat deposition in livestock. Cell adhesion molecule 2 (CADM2) is expressed widely in the brain and adipose tissue and can regulate body weight through the central nervous system. Growth traits are important economic traits for animal selection. In this study, we aimed to explore the effect of CADM2 gene copy number variants on yak growth traits. Here, two CNVs in the CADM2 gene were investigated using the quantitative polymerase chain reaction (qPCR), and the association of the CNVs with growth traits in yak was analyzed using statistical methods by SPSS software. Differences were considered significant if the p value was < 0.05. Statistical analysis indicated significant association of CADM2-CNV2 with the body weight of the Chinese Ashidan yak. A significant effect of CNV2 (p < 0.05) was found on body weight at 6 months. In CNV2, the gain-type copy number variation exhibited greater performance than the other variants, with greater body weight observed at 6 months (p < 0.05). To the best of our knowledge, this is the first attempt to investigate the function of CADM2-CNVs and their association with growth traits in animals. This may be a useful candidate marker in marker-assisted selection of yaks.


Author(s):  
Charles Lee ◽  
Stephen W. Scherer

During the past five years, copy number variation (CNV) has emerged as a highly prevalent form of genomic variation, bridging the interval between long-recognised microscopic chromosomal alterations and single-nucleotide changes. These genomic segmental differences among humans reflect the dynamic nature of genomes, and account for both normal variations among us and variations that predispose to conditions of medical consequence. Here, we place CNVs into their historical and medical contexts, focusing on how these variations can be recognised, documented, characterised and interpreted in clinical diagnostics. We also discuss how they can cause disease or influence adaptation to an environment. Various clinical exemplars are drawn out to illustrate salient characteristics and residual enigmas of CNVs, particularly the complexity of the data and information associated with CNVs relative to that of single-nucleotide variation. The potential is immense for CNVs to explain and predict disorders and traits that have long resisted understanding. However, creative solutions are needed to manage the sudden and overwhelming burden of expectation for laboratories and clinicians to assay and interpret these complex genomic variations as awareness permeates medical practice. Challenges remain for understanding the relationship between genomic changes and the phenotypes that might be predicted and prevented by such knowledge.


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