Author ORCID Identifier

N/A

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https://orcid.org/0000-0002-3964-5987

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Document Type

Article

Publication Date

2018

College/Unit

School of Medicine

Department/Program/Center

Neurology

Abstract

Photoreceptor cells are specialized neurons with a sensory cilium carrying an elaborate membrane structure, the outer segment (OS). Inherited mutations in genes involved in ciliogenesis frequently result in OS malformation and blindness. ADP-ribosylation factor-like 2 (ARL2) has recently been implicated in OS formation through its association with Binder of ARL2 (BART or ARL2BP), a protein linked to inherited blinding disease. To test the role of ARL2 in vision we created a transgenic mouse model expressing a tagged-dominant active form of human ARL2 (ARL2-Q70L) under a rod-specific promoter. Transgenic ARL2-Q70L animals exhibit reduced photoreceptor cell function as early as post-natal day 16 and progressive rod degeneration. We attribute loss of photoreceptor function to the defective OS morphogenesis in the ARL2-Q70L transgenic model. ARL2-Q70L expression results in shortened inner and outer segments, shortened and mislocalized axonemes and cytoplasmic accumulation of rhodopsin. In conclusion, we show that ARL2-Q70L is crucial for photoreceptor neuron sensory cilium development. Future research will expand upon our hypothesis that ARL2-Q70L mutant interferes with microtubule maintenance and tubulin regulation resulting in impaired growth of the axoneme and elaboration of the photoreceptor outer segment.

Source Citation

Wright, Z. C., Loskutov, Y., Murphy, D., Stoilov, P., Pugacheva, E., Goldberg, A. F. X., & Ramamurthy, V. (2018). ADP-Ribosylation Factor-Like 2 (ARL2) regulates cilia stability and development of outer segments in rod photoreceptor neurons. Scientific Reports, 8(1). https://doi.org/10.1038/s41598-018-35395-3

Comments

Open Access This article is licensed under a Creative Commons Attribution 4.0 International

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© The Author(s) 2018

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