A network comprising short and long noncoding RNAs and RNA helicase controls mouse retina architecture

Jacek Krol (), Ilona Krol, Claudia Patricia Patino Alvarez, Michele Fiscella, Andreas Hierlemann, Botond Roska () and Witold Filipowicz ()
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Jacek Krol: Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research
Ilona Krol: Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research
Claudia Patricia Patino Alvarez: Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research
Michele Fiscella: Bio Engineering Laboratory, ETH Zurich
Andreas Hierlemann: Bio Engineering Laboratory, ETH Zurich
Botond Roska: Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research
Witold Filipowicz: Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract Brain regions, such as the cortex and retina, are composed of layers of uniform thickness. The molecular mechanism that controls this uniformity is not well understood. Here we show that during mouse postnatal development the timed expression of Rncr4, a retina-specific long noncoding RNA, regulates the similarly timed processing of pri-miR-183/96/182, which is repressed at an earlier developmental stage by RNA helicase Ddx3x. Shifting the timing of mature miR-183/96/182 accumulation or interfering with Ddx3x expression leads to the disorganization of retinal architecture, with the photoreceptor layer being most affected. We identify Crb1, a component of the adhesion belt between glial and photoreceptor cells, as a link between Rncr4-regulated miRNA metabolism and uniform retina layering. Our results suggest that the precise timing of glia–neuron interaction controlled by noncoding RNAs and Ddx3x is important for the even distribution of cells across layers.

Date: 2015
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DOI: 10.1038/ncomms8305

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