Abstract

The amylase gene (AMY), which codes for a starch-digesting enzyme in animals, underwent several gene copy number gains in humans (Perry et al., 2007), dogs (Axelsson et al., 2013), and mice (Schibler et al., 1982), possibly along with increased starch consumption during the evolution of these species. Here, we present comprehensive evidence for AMY copy number expansions that independently occurred in several mammalian species which consume diets rich in starch. We also provide correlative evidence that AMY gene duplications may be an essential first step for amylase to be expressed in saliva. Our findings underscore the overall importance of gene copy number amplification as a flexible and fast evolutionary mechanism that can independently occur in different branches of the phylogeny.

Highlights

  • Diet has been a significant adaptive force in shaping human and nonhuman primate variation (Hardy et al, 2015; Milton, 1981; Zhang et al, 2002)

  • Amylase copy number gains occurred in multiple mammalian lineages independently The human lineage-specific amylase gene duplications were initially thought to represent a unique case of evolutionary adaptation to increased starch consumption in humans (Perry et al, 2007)

  • The recent revelation that a similar increase in amylase gene copy number occurred in dogs (Axelsson et al, 2013; Ollivier et al, 2016) is remarkable since it shows that the same gene underwent bursts of gene copy number gains in two separate species independently

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Summary

Introduction

Diet has been a significant adaptive force in shaping human and nonhuman primate variation (Hardy et al, 2015; Milton, 1981; Zhang et al, 2002). We found lineage-specific retrotransposons located in similar proximity (0.8–4.2 kb upstream or downstream) to multiple amylase gene copies in human, mouse, rat, pig, and dog reference genomes (Figure 2B).

Results
Conclusion

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