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miR-181a/b control the assembly of visual circuitry by regulating retinal axon specification and growth
Sabrina Carrella1, Ylenia D'Agostino1, Sara Barbato1
1Telethon Institute of Genetics and Medicine, Via Campi Flegrei 34, Pozzuoli (Naples), 80078, Italy.
Abstract:
Connectivity and function of neuronal circuitry require the correct specification and growth of axons and dendrites. Here, we identify the microRNAs miR-181a and miR-181b as key regulators of retinal axon specification and growth. Loss of miR-181a/b in medaka fish (Oryzias latipes) failed to consolidate amacrine cell processes into axons and delayed the growth of retinal ganglion cell (RGC) axons. These alterations were accompanied by defects in visual connectivity and function. We demonstrated that miR-181a/b exert these actions through negative modulation of MAPK/ERK signaling that in turn leads to RhoA reduction and proper neuritogenesis in both amacrine cells and RGCs via local cytoskeletal rearrangement. Our results identify a new pathway for axon specification and growth unraveling a crucial role of miR-181a/b in the proper establishment of visual system connectivity and function.
Insights
MicroRNAs miR-181a and miR-181b are crucial for retinal axon development. Their absence impairs visual system connectivity and function by affecting neuronal growth and signaling pathways.
Area of Science:
- Neuroscience
- Molecular Biology
- Developmental Biology
Background:
- Neuronal circuitry and function depend on precise axon and dendrite development.
- MicroRNAs (miRNAs) are known regulators of gene expression with roles in cellular processes.
Purpose of the Study:
- To identify key regulators of retinal axon specification and growth.
- To elucidate the role of specific microRNAs in visual system development and function.
Main Methods:
- Utilized medaka fish (Oryzias latipes) as a model organism.
- Investigated the effects of miR-181a/b loss-of-function on retinal axon development.
- Analyzed alterations in neuronal connectivity and visual function.
- Examined the underlying molecular mechanisms involving MAPK/ERK signaling and RhoA.
Main Results:
- Loss of miR-181a/b disrupted amacrine cell axon consolidation and delayed retinal ganglion cell (RGC) axon growth.
- Defects in visual connectivity and function were observed in miR-181a/b deficient fish.
- miR-181a/b were shown to negatively modulate MAPK/ERK signaling, leading to RhoA reduction.
- This pathway facilitates proper neuritogenesis and cytoskeletal rearrangement in amacrine cells and RGCs.
Conclusions:
- miR-181a and miR-181b are essential regulators of retinal axon specification and growth.
- A novel pathway involving miR-181a/b, MAPK/ERK signaling, and RhoA in neuritogenesis is identified.
- These microRNAs play a critical role in establishing visual system connectivity and function.
