Generation of an Armcx1 Conditional Knockout Mouse

Armadillo repeat-containing X-linked protein-1 (Armcx1) is a poorly characterized transmembrane protein that regulates mitochondrial transport in neurons. Its overexpression has been shown to induce neurite outgrowth in embryonic neurons and to promote retinal ganglion cell (RGC) survival and axonal regrowth in a mouse optic nerve crush model. In order to evaluate the functions of endogenous Armcx1 in vivo, we have created a conditional Armcx1 knockout mouse line in which the entire coding region of the Armcx1 gene is flanked by loxP sites. This Armcx1<sup>fl</sup> line was crossed with mouse strains in which Cre recombinase expression is driven by the promoters for β-actin and Six3, in order to achieve deletion of Armcx1 globally and in retinal neurons, respectively. Having confirmed deletion of the gene, we proceeded to characterize the abundance and morphology of RGCs in Armcx1 knockout mice aged to 15 months. Under normal physiological conditions, no evidence of aberrant retinal or optic nerve development or RGC degeneration was observed in these mice. The Armcx1<sup>fl</sup> mouse should be valuable for future studies investigating mitochondrial morphology and transport in the absence of Armcx1 and in determining the susceptibility of Armcx1-deficient neurons to degeneration in the setting of additional heritable or environmental stressors.

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Publication Details

Journal
genesis
Published
2024-08-01
DOI
https://doi.org/10.1002/dvg.23615
Primary Topic
Mitochondrial Function and Pathology
Type
article
Field-Weighted Citation Impact
0.00

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article

Generation of an Armcx1 Conditional Knockout Mouse

Cora L. Bright, Howard M. Bomze, Sidney M. Gospe, Jeremy N. Kay et al.
genesis
Mitochondrial Function and Pathology
article

Generation of an Armcx1 Conditional Knockout Mouse

Cora L. Bright, Howard M. Bomze, Sidney M. Gospe, Jeremy N. Kay, Romain Cartoni, Mantu Bhaumik
article en

Abstract

Armadillo repeat-containing X-linked protein-1 (Armcx1) is a poorly characterized transmembrane protein that regulates mitochondrial transport in neurons. Its overexpression has been shown to induce neurite outgrowth in embryonic neurons and to promote retinal ganglion cell (RGC) survival and axonal regrowth in a mouse optic nerve crush model. In order to evaluate the functions of endogenous Armcx1 in vivo, we have created a conditional Armcx1 knockout mouse line in which the entire coding region of the Armcx1 gene is flanked by loxP sites. This Armcx1<sup>fl</sup> line was crossed with mouse strains in which Cre recombinase expression is driven by the promoters for β-actin and Six3, in order to achieve deletion of Armcx1 globally and in retinal neurons, respectively. Having confirmed deletion of the gene, we proceeded to characterize the abundance and morphology of RGCs in Armcx1 knockout mice aged to 15 months. Under normal physiological conditions, no evidence of aberrant retinal or optic nerve development or RGC degeneration was observed in these mice. The Armcx1<sup>fl</sup> mouse should be valuable for future studies investigating mitochondrial morphology and transport in the absence of Armcx1 and in determining the susceptibility of Armcx1-deficient neurons to degeneration in the setting of additional heritable or environmental stressors.

genesisVol. 62(4)
Boston Children's Hospital (US), Harvard University (US), Duke University (US)
Research to Prevent Blindness, National Institutes of Health, Intellectual and Developmental Disabilities Research Center
Life in Land
Openalex Percentile: Top 88%
Mitochondrial Function and Pathology
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Generation of an Armcx1 Conditional Knockout Mouse — Cora L. Bright, Howard M. Bomze, et al. · genesis (2024) | TGRS Research Map | TGRS