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lncRNA - Long Non-coding RNAs

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...

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Differentiation of a Human Neural Stem Cell Line on Three Dimensional Cultures, Analysis of MicroRNA and Putative Target Genes

Differentiation of a Human Neural Stem Cell Line on Three Dimensional Cultures, Analysis of MicroRNA and Putative Target Genes

Published on: April 12, 2015

Roles of SNORD115 and SNORD116 ncRNA clusters during neuronal differentiation.

Aleksandra Helwak¹, Tomasz Turowski^2,3, Christos Spanos²

¹Institute for Cell Biology, School of Biological Sciences, The University of Edinburgh, Edinburgh, Scotland. ahelwak@ed.ac.uk.

Nature Communications

|November 30, 2024

Summary

Loss of SNORD116, but not SNORD115, is linked to Prader-Willi syndrome. This study reveals SNORD116 loss impacts neuronal development and RNA stability, offering insights into neurodevelopmental disorders.

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Area of Science:

Genetics
Neuroscience
Molecular Biology

Background:

The snoRNA host gene SNHG14 produces SNORD116 and SNORD115 from consecutive and tandem introns, respectively.
Loss of SNORD116 expression is associated with Prader-Willi syndrome, a neurodevelopmental disorder.
SNORD116 and SNORD115 are structurally similar to box C/D small nucleolar RNAs (snoRNAs) but lack identified targets.

Purpose of the Study:

To investigate the functional roles of SNORD116 and SNORD115 in neuronal development.
To elucidate the distinct mechanisms of SNORD115 and SNORD116 accumulation during neuronal differentiation.
To characterize the consequences of SNORD116 or SNORD115 cluster loss on cellular processes.

Main Methods:

Generation of cell lines lacking either the SNORD115 or SNORD116 cluster.
Analysis of RNA stability and protein synthesis during neuronal development in mutant cell lines.
Comparative analysis of mRNA and non-coding RNA alterations in SNORD115 and SNORD116 mutants.

Main Results:

Loss of SNORD116, not SNORD115, impacts neuronal cell developmental timing and RNA stability.
Distinct accumulation mechanisms were observed for SNORD115 (host-gene expression) and SNORD116 (stabilization) during neuronal differentiation.
Altered mRNAs include MAGEL2, associated with Schaaf-Yang syndrome, and protocadherins, crucial for neurodevelopmental cell signaling.

Conclusions:

SNORD116 plays a critical role in regulating neuronal development, with its loss potentially contributing to Prader-Willi syndrome phenotypes.
The study highlights differential regulation and functional importance of SNORD115 and SNORD116.
Identified altered RNAs and pathways provide potential molecular links between SNORD gene function and neurodevelopmental disorders.