Cancer gene also coordinates retina growth

A gene, which also behaves as a cancer precursor, has also been found to play a central role in the coordination of retinal proliferation and eye growth during foetal development, according to a report published in the January issue of Genes & Development.

The research led my Michael Dyer and colleagues from St Jude Children's Research Hospital, Memphis, Tennessee, USA discovered that the gene N-myc coordinates the growth of the retina and other eye structures to ensure the retina has the proper thickness necessary to convert light from the lens into nerve impulses that the brain transforms into images.

Genes in the Myc family carry out various vital roles during prenatal development by regulating the proliferation, size, differentiation and survival of cells. Myc genes are also proto-oncogenes, in which a mutation enables them to transform normal cells into cancerous ones. Malfunctioning N-myc genes are often associated with paediatric neural cancers, including neuroblastoma, medulloblastoma and retinoblastoma.

During the course of the research, it was found that N-myc is not involved in regulating cell survival or neuronal differentiation in the developing retina. However, the gene is crucial for the proper proliferation of retinal cells. The researchers deactivated the N-myc gene in mice and found that the volume of the retina was significantly smaller than in mice with the normally functioning M-myc.

The team found no evidence of an increase in progenitor cell deaths between normal and N-myc-deficient retinas, so it was concluded that the smaller retinas had probably resulted from an N-myc related proliferation defect in the progenitor retinal cells.

Overall, the team felt that N-myc's activity occurred early in the cascade of reactions controlling the development of the retina and other ocular components.

This is the first study to report on the molecular mechanisms responsible for the correct sizing of the retina, which was previously not understood.