Frequent Loss and Alteration of the MOXD2 Gene in Catarrhines and Whales: A Possible Connection with the Evolution of Olfaction

Kim, Dong Seon; Wang, Yao; Oh, Hye Ji; Lee, Kangseok; Hahn, Yoonsoo

doi:10.1371/journal.pone.0104085

Cited by 9 publications

(14 citation statements)

References 69 publications

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“…MOXD2 encodes a monooxygenase dopamine β-hydroxylase (DBH)-like 2 protein, and highly orthologous proteins are found in vertebrates [ 1 , 2 ]. MOXD2 and its paralogs, MOXD1 and DBH, are members of a copper type II, ascorbate-dependent monooxygenase family, which was formed by sequential duplication during bilaterian evolution [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

“…Human MOXD2 has a genomic deletion that spans 2 exons, which occurred after humans and chimpanzees diverged [ 1 ]. Orangutan MOXD2 has multiple nonsense mutations, and the gene has been completely deleted in gibbons [ 2 ]. Primates, especially Old World monkeys and apes, have enhanced visual perception, and they are less dependent on olfactory perception, which might have resulted in diminished olfaction and inactivation of olfaction-related genes [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

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MOXD2, a Gene Possibly Associated with Olfaction, Is Frequently Inactivated in Birds

et al. 2016

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Vertebrate MOXD2 encodes a monooxygenase DBH-like 2 protein that could be involved in neurotransmitter metabolism, potentially during olfactory transduction. Loss of MOXD2 in apes and whales has been proposed to be associated with evolution of olfaction in these clades. We analyzed 57 bird genomes to identify MOXD2 sequences and found frequent loss of MOXD2 in 38 birds. Among the 57 birds, 19 species appeared to have an intact MOXD2 that encoded a full-length protein; 32 birds had a gene with open reading frame-disrupting point mutations and/or exon deletions; and the remaining 6 species did not show any MOXD2 sequence, suggesting a whole-gene deletion. Notably, among 10 passerine birds examined, 9 species shared a common genomic deletion that spanned several exons, implying the gene loss occurred in a common ancestor of these birds. However, 2 closely related penguin species, each of which had an inactive MOXD2, did not share any mutation, suggesting an independent loss after their divergence. Distribution of the 38 birds without an intact MOXD2 in the bird phylogenetic tree clearly indicates that MOXD2 loss is widespread and independent in bird lineages. We propose that widespread MOXD2 loss in some bird lineages may be implicated in the evolution of olfactory perception in these birds.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MOXD2, a Gene Possibly Associated with Olfaction, Is Frequently Inactivated in Birds

et al. 2016

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“…The MOXD2 gene is also inactive in other apes: orangutans have multiple nonsense mutations and gibbons do not have the gene due to a genomic deletion that occurred in a common ancestor of all contemporary gibbons (21 , 70) . The gorilla gene shows an elevated non-synonymous substitution rate/synonymous substitution rate ratio, perhaps because its selection pressure has been recently relaxed, while the chimpanzee gene appears to be under purifying selection.…”

Section: Loss Of Olfaction-related Genes and Evolution Of Chemical Sementioning

confidence: 99%

“…Interestingly, MOXD2 gene inactivation also occurred in another mammalian clade, the Cetacea (70) . The dolphin and whale MOXD2 genes underwent a broad range of disruptive mutations, including nonsense, frameshift, and complete deletion.…”

Section: Loss Of Olfaction-related Genes and Evolution Of Chemical Sementioning

confidence: 99%

Loss of gene function and evolution of human phenotypes

Choi

Goh

et al. 2015

BMB Reports

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Humans have acquired many distinct evolutionary traits after the human-chimpanzee divergence. These phenotypes have resulted from genetic changes that occurred in the human genome and were retained by natural selection. Comparative primate genome analyses reveal that loss-of-function mutations are common in the human genome. Some of these gene inactivation events were revealed to be associated with the emergence of advantageous phenotypes and were therefore positively selected and fixed in modern humans (the “less-ismore” hypothesis). Representative cases of human gene inactivation and their functional implications are presented in this review. Functional studies of additional inactive genes will provide insight into the molecular mechanisms underlying acquisition of various human-specific traits. [BMB Reports 2015; 48(7): 373-379]

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“…The gain of new N-glycosylation sites during evolution may affect the structure and molecular function of proteins; when these novel modifications confer beneficial traits, they will be fixed during evolution. Previously, we identified a large variety of genetic changes that could have been involved in the acquisition of human traits, including gene inactivation [ 11 , 12 ], exon evolution [ 13 , 14 ], and gains of phosphorylation or ubiquitylation [ 15 , 16 ]. Therefore, it would be of great interest to collect information on novel N-glycosylation sites that arose during human evolution, as the sites might have been involved in the development of some human phenotypes.…”

Section: Introductionmentioning

confidence: 99%

The acquisition of novel N-glycosylation sites in conserved proteins during human evolution

Kim

Hahn

2015

BMC Bioinformatics

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BackgroundN-linked protein glycosylation plays an important role in various biological processes, including protein folding and trafficking, and cell adhesion and signaling. The acquisition of a novel N-glycosylation site may have significant effect on protein structure and function, and therefore, on the phenotype.ResultsWe analyzed the human glycoproteome data set (2,534 N-glycosylation sites in 1,027 proteins) and identified 112 novel N-glycosylation sites in 91 proteins that arose in the human lineage since the last common ancestor of Euarchonta (primates and treeshrews). Three of them, Asn-196 in adipocyte plasma membrane-associated protein (APMAP), Asn-91 in cluster of differentiation 166 (CD166/ALCAM), and Asn-76 in thyroglobulin, are human-specific. Molecular evolutionary analysis suggested that these sites were under positive selection during human evolution. Notably, the Asn-76 of thyroglobulin might be involved in the increased production of thyroid hormones in humans, especially thyroxine (T4), because the removal of the glycan moiety from this site was reported to result in a significant decrease in T4 production.ConclusionsWe propose that the novel N-glycosylation sites described in this study may be useful candidates for functional analyses to identify innovative genetic modifications for beneficial phenotypes acquired in the human lineage.Electronic supplementary materialThe online version of this article (doi:10.1186/s12859-015-0468-5) contains supplementary material, which is available to authorized users.

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Frequent Loss and Alteration of the MOXD2 Gene in Catarrhines and Whales: A Possible Connection with the Evolution of Olfaction

Cited by 9 publications

References 69 publications

MOXD2, a Gene Possibly Associated with Olfaction, Is Frequently Inactivated in Birds

MOXD2, a Gene Possibly Associated with Olfaction, Is Frequently Inactivated in Birds

Loss of gene function and evolution of human phenotypes

The acquisition of novel N-glycosylation sites in conserved proteins during human evolution

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