Alfyfl/fl floxed mice have loxP sites flanking exon 5 of the WD repeat and FYVE domain containing 3 (WDFY3) gene. Wdfy3 encodes ALFY, a phosphatidylinositol 3-phosphate-binding protein that shuttles from the nuclear membrane to colocalize with aggregated proteins, where it complexes with other autophagic components to achieve macroautophagy-mediated clearance of these aggregated proteins. Autophagy is impaired in Huntington's disease (HD) patients, and this impairment contributes to the accumulation of mutant huntingtin (mHTT) protein and its aggregates. A SNP in human WDFY3 was discovered in a family in Venezuela that was associated with a delayed age of onset Huntington's disease (HD) of up to 23 years. Homozygous Alfyfl/fl mice are viable and fertile. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 5 deleted in the cre-expressing tissues. Cre-activity generates a 66 amino acid truncated non-functional knock-out allele, no ALFY protein is detected. These mice may be useful when studying the role of ALFY in protecting against neurotoxicity in proteinopathies including Huntington's disease (HD), Alzheimer's disease (AD), Parkinson's disease (PD), and ALS with frontotemporal dementia.

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Alfyfl floxed mice have loxP sites flanking exon 5 of the Wdfy3 gene. These mice may be useful when studying the role of ALFY in protecting against neurotoxicity in proteinopathies including Huntington's disease (HD), Alzheimer's disease (AD), Parkinson's disease (PD), and ALS with frontotemporal dementia.