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Localisation of the putative magnetoreceptive protein Cryptochrome 1b in the retinae of migratory birds and homing pigeons

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Günther,  Anja       
Department of Computational Neuroethology, Max Planck Institute for Neurobiology of Behavior – caesar, Max Planck Society;
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Citation

Bolte, P., Bleibaum, F., Einwich, A., Günther, A., Liedvogel, M., Heyers, D., et al. (2016). Localisation of the putative magnetoreceptive protein Cryptochrome 1b in the retinae of migratory birds and homing pigeons. PLOS ONE, 11(3): e0147819. doi:10.1371/journal.pone.0147819.


Cite as: https://hdl.handle.net/21.11116/0000-0011-5A34-E
Abstract
Cryptochromes are ubiquitously expressed in various animal tissues including the retina. Some cryptochromes are involved in regulating circadian activity. Cryptochrome proteins have also been suggested to mediate the primary mechanism in light-dependent magnetic compass orientation in birds. Cryptochrome 1b (Cry1b) exhibits a unique carboxy terminus exclusively found in birds so far, which might be indicative for a specialised function. Cryptochrome 1a (Cry1a) is so far the only cryptochrome protein that has been localised to specific cell types within the retina of migratory birds. Here we show that Cry1b, an alternative splice variant of Cry1a, is also expressed in the retina of migratory birds, but it is primarily located in other cell types than Cry1a. This could suggest different functions for the two splice products. Using diagnostic bird-specific antibodies (that allow for a precise discrimination between both proteins), we show that Cry1b protein is found in the retinae of migratory European robins (Erithacus rubecula), migratory Northern Wheatears (Oenanthe oenanthe) and pigeons (Columba livia). In all three species, retinal Cry1b is localised in cell types which have been discussed as potentially well suited locations for magnetoreception: Cry1b is observed in the cytosol of ganglion cells, displaced ganglion cells, and in photoreceptor inner segments. The cytosolic rather than nucleic location of Cry1b in the retina reported here speaks against a circadian clock regulatory function of Cry1b and it allows for the possible involvement of Cry1b in a radical-pair-based magnetoreception mechanism.