Chx10-LNL-DTA knock-in/knock-out mice have a loxP-flanked stop sequence and an attenuated form of the Diphtheria Toxin A-chain (DTA) gene (fragment (tox-176)) inserted into the promotor at the ATG of the visual system homeobox 2 (Vsx2) gene. Insertion of LNL-DTA abolishes endogenous Vsx2 gene expression. Vsx2 encodes a transcriptional regulator essential for establishing retinal progenitor cell identity. It is also expressed in neurons present in the brainstem and spinal cord (called V2a neurons) which are important for coordinating motor activity. Mice that are homozygous for this allele are viable and fertile and exhibit microphthalmia, while mice heterozygous for this allele do not exhibit microphthalmia. When Chx10-LNL-DTA mice are crossed with a strain expressing Cre recombinase, deletion of the loxP-flanked stop sequence will result in the expression of diphtheria toxin in the Cre- and Csx2-expressing cells of the offspring, killing those cells. When Chx10-LNL-DTA mice are crossed to Prm-cre mice (see Stock No. <a href="https://www.jax.org/strain/003328">003328</a>), recombination in the male germline of results in expression of diphtheria toxin in all Vsx2 neurons in the eye, brainstem and spinal cord. Specifically, the number of Chx10+ neurons is dramatically reduced in the lumbar spinal cord of Chx10-DTA embryos at E11.5 compared with that of wild-type littermates, however, the number and location of V0 neurons that drive left-right alternation, inhibitory V2b interneurons, and motor neurons is not altered. Chx10-DTA mice show a progressive loss of Chx10+ neurons that is complete prior to P0.

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Chx10-LNL-DTA knock-in/knock-out mice have a loxP-flanked stop sequence and an attenuated form of the DTA gene (fragment (tox-176)) inserted into the promotor at the ATG of the Vsx2 gene. They may be useful for studying retinal progenitor cells during retinal development and motor coordination.

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