Copy Number Variation of the CADM2 Gene and Its Association with Growth Traits in Yak.

Fei Ge,Congjun Jia,Chunnian Liang,Min Chu,Ping Yan

doi:10.3390/ani9121008

Abstract

Simple SummaryCell adhesion molecule 2 (CADM2), also known as synaptic cell adhesion molecule 2 (SYNCAM2), is the mediator of synaptic signals enriched in the brain. Overlaps between copy number variation (CNV) regions in CADM2 and quantitative trait loci (QTL) related to body weight have been clarified in a previous study. In this study, two loci were amplified in the CADM2 gene (CNV1: 235,915 bp, exon 1 and partial intron 1; CNV2: 60,430 bp, intron 9) to explore the relationship between CNV types in the CADM2 gene and growth traits in 350 Ashidan yaks. Association analysis illustrated that no significant effect was found on growth traits in CNV1. However, the CNV2 mutation had a significant effect on body weight at the sixth month (p < 0.05). Individuals with the gain-type copy number variation CNV2 were significantly superior to those with loss- or normal-type in terms of body weight (p < 0.05). In summary, this study confirmed that CADM2-CNVs affect growth traits in yaks, and may be candidate genes for successful yak breeding and genetics projects. 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.

Highlights

With large duplications and deletions in gene copy numbers detected in humans and other primates, it is not unreasonable to expect that copy number variation could be a significant source of genetic variation in other animals [1]
The present study investigated the interrelations of copy number variation (CNV) including CNV1 (235,915 bp, exon 1 and partial intron 1) and CNV2 (60,430 bp, intron 9) with the Cell adhesion molecule 2 (CADM2) gene with growth traits in the yak, by performing quantitative real-time polymerase chain reaction (PCR)
Because of the importance of both the CADM2 gene and copy number variance in animals, we propose that CADM2-CNVs can be used as indispensable molecular markers of genetic improvement of the yak

Summary

Introduction

With large duplications and deletions in gene copy numbers detected in humans and other primates, it is not unreasonable to expect that copy number variation could be a significant source of genetic variation in other animals [1]. Many molecular markers have been assessed for improving economic traits in animal breeding, including restriction fragment length. Animals 2019, 9, 1008 polymorphisms (RFLP), single nucleotide polymorphisms (SNP), indels (Insertion/Deletion) and structural variations, such as inversions, duplications and deletions. More than 99% of indels are less than 50 bp in length [6,7], and some long insertions and deletions are returned into the concept of structural variation [8]. CNVs include duplication and/or deletions of DNA fragments ≥50 kb, and can cause a greater number of differences than SNPs and indels [12], which can be discovered by clone-based array comparative genome hybridization (array-CGH) [13]. Copy number variants can be engendered through four mechanisms: non-allelic homologous recombination (NAHR), non-homologous end joining (NHEJ), fork stalling and template switching (FoSTeS), and

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