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| Cell type-specific effects of Rb deletion in the murine retina |
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| Author(s): MacPherson D, Sage J, Kim T, Ho D, McLaughlin ME, Jacks T |
| Source: GENES & DEVELOPMENT Volume: 18 Issue: 14 Pages: 1681-1694 Published: JUL 15 2004 |
| Times Cited: 85 References: 61 |
| Abstract: Certain cells of the human retina are extremely sensitive to loss of function of the retinoblastoma tumor suppressor gene RB. Retinoblastomas develop early in life and at high frequency in individuals heterozygous for a germ-line RB mutation, and sporadic retinoblastomas invariably have somatic mutation in the PB gene. In contrast, retinoblastomas do not develop in Rb+/- mice. Although retinoblastoma is thought to have developmental origins, the function of Rb in retinal development has not been fully characterized. Here we studied the role of Rb in normal retinal development and in retinoblastoma using conditional Rb mutations in the mouse. In late embryogenesis, Rb-deficient retinas exhibited ectopic S-phase and high levels of p53-independent apoptosis, particularly in the differentiating retinal ganglion cell layer. During postnatal retinal development, loss of Rb led to more widespread retinal apoptosis, and adults showed loss of photoreceptors and bipolar cells. Conditional Rb mutation in the retina did not result in retinoblastoma formation even in a p53-mutant background. However, on a p107- or p130-deficient background, Rb mutation in the retina caused retinal dysplasia or retinoblastoma. |
| Document Type: Article |
| Language: English |
| Reprint Address: Jacks, T (reprint author), MIT, Dept Biol, 77 Massachusetts Ave, Cambridge, MA 02139 USA |
Addresses:
1. MIT, Dept Biol, Cambridge, MA 02139 USA
2. MIT, Canc Res Ctr, Cambridge, MA 02139 USA
3. Howard Hughes Med Inst, Chevy Chase, MD 20185 USA |
| Publisher: COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA |
| Subject Category: Cell Biology; Developmental Biology; Genetics & Heredity |
| IDS Number: 838VT |
| ISSN: 0890-9369 |
| DOI: 10.1101/gad.1203304 |
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