Hts, the Drosophila Homologue of Adducin, Physically Interacts With the 
Transmembrane Receptor Golden Goal to Guide Photoreceptor Axons

Ohler, S.; Hakeda-Suzuki, S.; Suzuki, T.

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Hts, the Drosophila Homologue of Adducin, Physically Interacts With the Transmembrane Receptor Golden Goal to Guide Photoreceptor Axons

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Ohler, S.
Max Planck Research Group: Axonal Guidance and Neuronal Connectivity / Suzuki, MPI of Neurobiology, Max Planck Society;

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Hakeda-Suzuki, S.
Max Planck Research Group: Axonal Guidance and Neuronal Connectivity / Suzuki, MPI of Neurobiology, Max Planck Society;

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Suzuki, T.
Max Planck Research Group: Axonal Guidance and Neuronal Connectivity / Suzuki, MPI of Neurobiology, Max Planck Society;

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引用

Ohler, S., Hakeda-Suzuki, S., & Suzuki, T. (2011). Hts, the Drosophila Homologue of Adducin, Physically Interacts With the Transmembrane Receptor Golden Goal to Guide Photoreceptor Axons. Developmental Dynamics, 240(1), 135-148.

引用: https://hdl.handle.net/11858/00-001M-0000-0012-1F1D-1

要旨

Neurons steer their axons towards their proper targets during development. Molecularly, a number of guidance receptors have been identified. The transmembrane protein Golden goal (Gogo) was reported previously to guide photoreceptor (R) axons in the Drosophila visual system. Here, we show that Hts, the Drosophila homologue of Adducin, physically interacts with Gogo's cytoplasmic domain via its head-neck domain. hts null mutants show similar defects in R axon guidance as do gogo mutants. Rescue experiments suggest that the C-terminal tail but not the MARCKS homology domain of Hts is required. Overexpression of either gogo or hts causes abnormally thick swellings of R8 axons in the medulla, but if both are co-overexpressed, R8 axons appear normal and the amount of excessive Hts is reduced. Our results fit with a model where Gogo both positively and negatively regulates Hts that affects the Actin-Spectrin cytoskeleton in growth cone filopodia, thereby guiding R axons. Developmental Dynamics 240: 135-148, 2011. (C) 2010 Wiley-Liss, Inc.