Abstract
Amacrine cells (ACs) are the most diverse neuronal cell type in the vertebrate retina. Yet little is known about the contribution of ACs to visual processing and retinal disease. A major challenge in evaluating AC function is genetic accessibility. A classic tool of mouse genetics, Cre-mediated recombination, can provide such access. We have screened existing genetically-modified mouse strains and identified multiple candidates that express Cre-recombinase in subsets of retinal ACs. The Cre-expressing mice were crossed to fluorescent-reporter mice to assay Cre expression. In addition, a Cre-dependent fluorescent reporter plasmid was electroporated into the subretinal space of Cre strains. Herein, we report 3 mouse lines (Tac1::IRES-cre, Camk2a-cre, and Scx-cre that express Cre recombinase in sub-populations of ACs. In 2 of these lines, recombination occurred in multiple AC types and a small number of other retinal cell types, while recombination in the Camk2a-cre line appears specific to a morphologically distinct AC. We anticipate that these characterized mouse lines will be valuable tools to the community of researchers who study retinal biology and disease.
Significance
Amacrine cells (ACs) are highly diverse, inhibitory interneurons of the retina. The roles of the majority of these ACs are poorly understood, particularly in terms of their role in visual processing and retinal disease. The present study describes 3 mouse strains with Cre-recombinase expression in specific subpopulations of ACs. As Cre-loxP constructs allow efficient labeling and manipulation of cells in vivo, we anticipate that the mouse models will be valuable tools in the study of AC biology.
Footnotes
Authors report no conflict of interest.
This project was supported by Howard Hughes Medical Institute (to C.L.C, D.G.A. and W.Y.)
This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
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