Gene expression profiling of light-induced retinal degeneration in phototransduction gene knockout mice.
10.3858/emm.2008.40.5.495
- Author:
Jayalakshmi KRISHNAN
1
;
Jiayan CHEN
;
Kum Joo SHIN
;
Jong Ik HWANG
;
Sang Uk HAN
;
Gwang LEE
;
Sangdun CHOI
Author Information
1. Department of Molecular Science and Technology, Ajou University, Suwon, Korea. glee@ajou.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
arrestin;
gene expression profiling;
oligonucleotide array sequence analysis;
proto-oncogene proteins c-fos;
retinal degeneration;
transducin
- MeSH:
Animals;
Apoptosis/radiation effects;
G-Protein-Coupled Receptor Kinase 1/genetics;
GTP-Binding Protein alpha Subunits/genetics;
*Gene Expression Profiling;
Genes, fos/genetics;
Light/adverse effects;
Light Signal Transduction/*genetics/physiology/radiation effects;
Mice;
Mice, Knockout;
Oligonucleotide Array Sequence Analysis;
Retina/metabolism/pathology/radiation effects;
Retinal Degeneration/etiology/*genetics/physiopathology;
Transducin/genetics
- From:Experimental & Molecular Medicine
2008;40(5):495-504
- CountryRepublic of Korea
- Language:English
-
Abstract:
Exposure to light can induce photoreceptor cell death and exacerbate retinal degeneration. In this study, mice with genetic knockout of several genes, including rhodopsin kinase (Rhok-/-), arrestin (Sag-/-), transducin (Gnat1-/-), c-Fos (c-Fos-/-) and arrestin/transducin (Sag-/-/Gnat1-/-), were examined. We measured the expression levels of thousands of genes in order to investigate their roles in phototransduction signaling in light-induced retinal degeneration using DNA microarray technology and then further explored the gene network using pathway analysis tools. Several cascades of gene components were induced or inhibited as a result of corresponding gene knockout under specific light conditions. Transducin deletion blocked the apoptotic signaling induced by exposure to low light conditions, and it did not require c-Fos/AP-1. Deletion of c-Fos blocked the apoptotic signaling induced by exposure to high intensity light. In the present study, we identified many gene transcripts that are essential for the initiation of light-induced rod degeneration and proposed several important networks that are involved in pro- and anti-apoptotic signaling. We also demonstrated the different cascades of gene components that participate in apoptotic signaling under specific light conditions.
