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Loss of Irrk2 impairs cell proliferation and neuronal regeneration in the zebrafish brain

Stefano Suzzi, Reiner Ahrendt, Stefan Hans, Svetlana A. Semenova, Saygin Bilican, Shady Sayed, Sylke Winkler, Sandra Spieß, Jan Kaslin, Pertti Panula, Michael Brand
doi: https://doi.org/10.1101/140608
Stefano Suzzi
1Biotechnology Center (BIOTEC) and Center for Regenerative Therapies Technische Universität Dresden (CRTD), Dresden, Germany
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Reiner Ahrendt
1Biotechnology Center (BIOTEC) and Center for Regenerative Therapies Technische Universität Dresden (CRTD), Dresden, Germany
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Stefan Hans
1Biotechnology Center (BIOTEC) and Center for Regenerative Therapies Technische Universität Dresden (CRTD), Dresden, Germany
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Svetlana A. Semenova
3Neuroscience Center, Institute of Biomedicine/Anatomy, University of Helsinki, Helsinki, Finland
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Saygin Bilican
1Biotechnology Center (BIOTEC) and Center for Regenerative Therapies Technische Universität Dresden (CRTD), Dresden, Germany
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Shady Sayed
1Biotechnology Center (BIOTEC) and Center for Regenerative Therapies Technische Universität Dresden (CRTD), Dresden, Germany
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Sylke Winkler
2Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), Dresden, Germany
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Sandra Spieß
1Biotechnology Center (BIOTEC) and Center for Regenerative Therapies Technische Universität Dresden (CRTD), Dresden, Germany
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Jan Kaslin
1Biotechnology Center (BIOTEC) and Center for Regenerative Therapies Technische Universität Dresden (CRTD), Dresden, Germany
4present address: Australian Regenerative Medicine Institute, Monash University, Clayton, Australia
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Pertti Panula
3Neuroscience Center, Institute of Biomedicine/Anatomy, University of Helsinki, Helsinki, Finland
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Michael Brand
1Biotechnology Center (BIOTEC) and Center for Regenerative Therapies Technische Universität Dresden (CRTD), Dresden, Germany
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Abstract

LRRK2 mutations are a major cause of Parkinson’s disease. Pathogenicity of LRRK2 loss-of-function is controversial, as knockout in rodents induces no brain-specific effects and knockdown studies in zebrafish are conflicting. Here we show that deletion of the ~60-kbp-long zebrafish Irrk2 locus elicits a pleomorphic, albeit transient brain phenotype in maternal-zygotic mutants (mzLrrk2). Intriguingly, 11-month-old mzLrrk2 adults display increased amine catabolism. Additionally, we find decreased mitosis in the larval brain and reduced stab injury-induced neuronal regeneration in the adult telencephalon. Finally, hypokinesia associates with loss of Irrk2 in larvae. Our results demonstrate that Irrk2 knockout has an early neurodevelopmental effect. We report for the first time perturbed amine catabolism in a LRRK2 knockout. We propose mzLrrk2 zebrafish as a valuable tool to study LRRK2 loss-of-function in vivo, and provide a link between LRRK2 and the control of basal cell proliferation in the brain, potentially critical upon challenges like brain injury.

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Posted May 23, 2017.
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Loss of Irrk2 impairs cell proliferation and neuronal regeneration in the zebrafish brain
Stefano Suzzi, Reiner Ahrendt, Stefan Hans, Svetlana A. Semenova, Saygin Bilican, Shady Sayed, Sylke Winkler, Sandra Spieß, Jan Kaslin, Pertti Panula, Michael Brand
bioRxiv 140608; doi: https://doi.org/10.1101/140608
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Loss of Irrk2 impairs cell proliferation and neuronal regeneration in the zebrafish brain
Stefano Suzzi, Reiner Ahrendt, Stefan Hans, Svetlana A. Semenova, Saygin Bilican, Shady Sayed, Sylke Winkler, Sandra Spieß, Jan Kaslin, Pertti Panula, Michael Brand
bioRxiv 140608; doi: https://doi.org/10.1101/140608

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