Brn-3b inhibits generation of amacrine cells by binding to and negatively regulating DLX1/2 in developing retina
Copyright policy )Brn-3b inhibits generation of amacrine cells by binding to and negatively regulating DLX1/2 in developing retina
During retinogenesis, the basic helix-loop-helix proneural gene math5 (atoh7) initiates the generation of the first-born neurons, retinal ganglion cells (RGCs), by activating a network of RGC transcription factors, including Brn-3b (POU4F2). Herein, we show that the expression of DLX1 and DLX2 is significantly down-regulated in math5-null retina but is markedly increased in Brn-3b-null retina. Interestingly, Brn-3b interacts with DLX1 through its homeodomain, and this interaction represses DLX1 activity. Retrovirus-mediated mis-expression of DLX1 or DLX2 dramatically increases the number of amacrine/bipolar cells and concurrently reduces rod photoreceptors. Conversely, combined ectopic expression of Brn-3b with DLX1 or DLX2 promotes the production of RGCs and inhibits amacrine cell differentiation. Thus, DLX1/2 play an essential role in cell fate selection between amacrine and RGCs. Brn-3b suppresses the role of DLX1/2 through physical interaction and biases the competent precursors toward RGC fates.
- University of Tsukuba Japan
- Gunma University Japan
- University of Manitoba Canada
- University of Rochester United States
Homeodomain Proteins, Retinal Ganglion Cells, Neurogenesis, Blotting, Western, Gene Expression Regulation, Developmental, Cell Differentiation, Immunohistochemistry, Retina, Transcription Factor Brn-3B, Mice, Amacrine Cells, Neural Stem Cells, Animals, Immunoprecipitation, Gene Knock-In Techniques, In Situ Hybridization, Transcription Factors
Homeodomain Proteins, Retinal Ganglion Cells, Neurogenesis, Blotting, Western, Gene Expression Regulation, Developmental, Cell Differentiation, Immunohistochemistry, Retina, Transcription Factor Brn-3B, Mice, Amacrine Cells, Neural Stem Cells, Animals, Immunoprecipitation, Gene Knock-In Techniques, In Situ Hybridization, Transcription Factors
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