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First published online 5 November 2008
doi: 10.1242/dev.024620

Development 135, 3923-3933 (2008)
Published by The Company of Biologists 2008
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Temporal requirement of the alternative-splicing factor Sfrs1 for the survival of retinal neurons

Rahul N. Kanadia1,2, Victoria E. Clark1, Claudio Punzo1, Jeffrey M. Trimarchi1 and Constance L. Cepko1,2,3,*

1 Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
2 Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA.
3 Department of Ophthalmology, Harvard Medical School, Boston, MA 02115, USA.

* Author for correspondence (e-mail: cepko{at}genetics.med.harvard.edu)

Accepted 2 October 2008

Alternative splicing is the primary mechanism by which a limited number of protein-coding genes can generate proteome diversity. We have investigated the role of the alternative-splicing factor Sfrs1, an arginine/serine-rich (SR) protein family member, during mouse retinal development. Loss of Sfrs1 function during embryonic retinal development had a profound effect, leading to a small retina at birth. In addition, the retina underwent further degeneration in the postnatal period. Loss of Sfrs1 function resulted in the death of retinal neurons that were born during early to mid-embryonic development. Ganglion cells, cone photoreceptors, horizontal cells and amacrine cells were produced and initiated differentiation. However, these neurons subsequently underwent cell death through apoptosis. By contrast, Sfrs1 was not required for the survival of the neurons generated later, including later-born amacrine cells, rod photoreceptors, bipolar cells and Müller glia. Our results highlight the requirement of Sfrs1-mediated alternative splicing for the survival of retinal neurons, with sensitivity defined by the window of time in which the neuron was generated.

Key words: Alternative splicing, Sfrs1, Survival of retinal neurons, Temporal


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