| Functional |
"Although other forces and scenarios cannot be ruled out (33), an intriguing hypothesis is that the loss enabled the survival of Odontoceti ancestors from a virus that took advantage of Mx function, possibly through direct interaction with the Mx proteins [e.g., human individuals and cells that inactivate the CCR5 gene are resistant to HIV-1 infection (34)], or through mimicry of the Mx proteins (35)." |
10.1073/pnas.1501844112 |
| Mutation Description |
"For example, Mx1 loss was evidenced in bottlenose dolphin by: (i) a frameshifting deletion of exons 10–12 in the stalk domain, including the L4 loop; (ii) two additional frameshift mutations in exons 3 and 5 of the GTPase domain; and (iii) a Ka/Ks (nonsynonymous to synonymous substitution rate) using cow as a reference over twice as high as the
Ka/Ks from cow to human." |
10.1073/pnas.1501844112 |
| Methodology & Validation |
"Deletions were validated in sperm whale, killer whale, and bottlenose dolphin by finding at least three sequencing reads that aligned with at least 15 bases on either side of the deleted region. We converted the pairwise alignments for each exon to a multiple alignment using Muscle v3.8.31 with a strict gap opening penalty of −800 (49). Frameshift mutations and stop codons were validated by manually inspecting multiple alignments of each exon across human, cow, and the five cetaceans. Furthermore, frameshift mutations and stop codons occurring only in sperm whale, killer whale, or bottlenose dolphin were validated by finding at least three raw sequencing reads containing the mutation." |
10.1073/pnas.1501844112 |
| Timing of Loss |
"We trace the likely loss event for both proteins to soon after the divergence of Odontocetes and Mystocetes (baleen whales) ∼33–37 Mya." |
10.1073/pnas.1501844112 |