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The ancestral role of nodal signalling in breaking L/R symmetry in the vertebrate forebrain

Left-right asymmetries in the epithalamic region of the brain are widespread across vertebrates, but their magnitude and laterality varies among species. Whether these differences reflect independent origins of forebrain asymmetries or taxa-specific diversifications of an ancient vertebrate feature...

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Published in:Nature communications 2015-03, Vol.6 (1), p.6686-6686, Article 6686
Main Authors: Lagadec, Ronan, Laguerre, Laurent, Menuet, Arnaud, Amara, Anis, Rocancourt, Claire, Péricard, Pierre, Godard, Benoît G., Celina Rodicio, Maria, Rodriguez-Moldes, Isabel, Mayeur, Hélène, Rougemont, Quentin, Mazan, Sylvie, Boutet, Agnès
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Language:English
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Summary:Left-right asymmetries in the epithalamic region of the brain are widespread across vertebrates, but their magnitude and laterality varies among species. Whether these differences reflect independent origins of forebrain asymmetries or taxa-specific diversifications of an ancient vertebrate feature remains unknown. Here we show that the catshark Scyliorhinus canicula and the lampreys Petromyzon marinus and Lampetra planeri exhibit conserved molecular asymmetries between the left and right developing habenulae. Long-term pharmacological treatments in these species show that nodal signalling is essential to their generation, rather than their directionality as in teleosts. Moreover, in contrast to zebrafish, habenular left-right differences are observed in the absence of overt asymmetry of the adjacent pineal field. These data support an ancient origin of epithalamic asymmetry, and suggest that a nodal-dependent asymmetry programme operated in the forebrain of ancestral vertebrates before evolving into a variable trait in bony fish. The epithalamus exhibits left-right asymmetries with different magnitudes among vertebrates. Here, the authors show that the catshark and two lampreys have conserved molecular asymmetries between the left and right developing epithalamus which are controlled by nodal signalling.
ISSN:2041-1723
2041-1723
DOI:10.1038/ncomms7686