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. 2019 Sep 25;5(9):eaaw6671. doi: 10.1126/sciadv.aaw6671

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Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).

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Fig. 3 — (A and B) The loss of MAP3K19 (mitogen-activated protein kinase 19) and SEC14L3 (SEC14-like lipid binding 3), which are specifically expressed in cell types of the lung, may relate to the high-performance respiratory system of cetaceans. (C) The loss of the renal amino acid transporter SLC6A18 (solute carrier family 6 member 18) offers an explanation for the low plasma arginine levels in cetaceans and may have contributed to stronger vasoconstriction during the diving response. Visualization as in Fig. 1A. A shared donor (gt ➔ at) and acceptor (ag ➔ aa) splice site disrupting mutation is indicated in (B). All inactivating mutations are shown in figs. S7 to S9.