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The long noncoding RNA RNCR2 directs mouse retinal cell specification.

Nicole A Rapicavoli¹, Erin M Poth, Seth Blackshaw

¹Department of Neuroscience, Neurology and Ophthalmology, Center for High-Throughput Biology and Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 N, Broadway Avenue, Baltimore, MD, USA.

BMC Developmental Biology

|May 13, 2010

Summary

This summary is machine-generated.

The long noncoding RNA RNCR2 regulates mouse retinal cell differentiation. Its mislocalization causes increased amacrine cells and Müller glia, revealing its critical role in cell fate specification.

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Area of Science:

Neuroscience
Developmental Biology
RNA Biology

Background:

Long noncoding RNAs (lncRNAs) are abundant in the developing nervous system.
The functions of most lncRNAs, including in retinal development, remain largely unknown.

Purpose of the Study:

Investigate the function of the abundant lncRNA RNCR2 in mouse retinal cell differentiation.
Determine RNCR2's role in retinal cell fate specification.

Main Methods:

Selective expression analysis of RNCR2 in retinal progenitor and precursor cells.
Short hairpin RNA (shRNA)-mediated knockdown of RNCR2.
Fusion of RNCR2 with IRES-GFP to study nuclear export and overexpression effects.
Identification of functional domains within RNCR2 using the IRES-GFP fusion system.

Main Results:

RNCR2 is expressed in specific retinal progenitor and precursor cell populations.
RNCR2 knockdown increases amacrine cell and Müller glia numbers, indicating a role in cell fate.
Forced nuclear export of RNCR2 via IRES-GFP fusion mimics knockdown effects, suggesting a dominant-negative phenotype.
Specific RNCR2 domains were identified as crucial for repressing amacrine and Müller glial differentiation.

Conclusions:

The lncRNA RNCR2 is essential for regulating mammalian retinal cell fate specification.
A novel method for creating dominant-negative lncRNA constructs was developed, applicable for broader lncRNA functional studies.