biostudies-literatureChesney KLHHS | National Institutes of HealthNIH HHS269-281https://www.ebi.ac.uk/biostudies/studies/S-EPMC8285577biostudies-literatureUnknown53(6)<i>ATG16L1</i> is a ubiquitous autophagy gene responsible, in part, for formation of the double-membrane bound autophagosome that delivers unwanted cellular debris and intracellular pathogens to the lysosome for degradation. A single, nonsynonymous adenine to guanine polymorphism resulting in a threonine to alanine amino acid substitution (T300A) directly preceded by a caspase cleavage site (DxxD) causes an increased susceptibility to Crohn's disease (CD) in humans. The mechanism behind this increased susceptibility is still being elucidated, however, the amino acid change caused by this point mutation results in increased ATG16L1 protein sensitivity to caspase 3-mediated cleavage. To generate novel rat strains carrying genetic alterations in the rat <i>Atg16l1</i> gene, we first characterPhysiological genomicsThe <i>Atg16l1</i> gene: characterization of wild type, knock-in, and knock-out phenotypes in rats.PMC8285577T32 OD011126P40 OD011062-14S1P40 OD011062Men HBryda ECChesney KLHankins MAfalseThe <i>Atg16l1</i> gene: characterization of wild type, knock-in, and knock-out phenotypes in rats.<i>ATG16L1</i> is a ubiquitous autophagy gene responsible, in part, for formation of the double-membrane bound autophagosome that delivers unwanted cellular debris and intracellular pathogens to the lysosome for degradation. A single, nonsynonymous adenine to guanine polymorphism resulting in a threonine to alanine amino acid substitution (T300A) directly preceded by a caspase cleavage site (DxxD) causes an increased susceptibility to Crohn's disease (CD) in humans. The mechanism behind this increased susceptibility is still being elucidated, however, the amino acid change caused by this point mutation results in increased ATG16L1 protein sensitivity to caspase 3-mediated cleavage. To generate novel rat strains carrying genetic alterations in the rat <i>Atg16l1</i> gene, we first character2021-01-01T00:00:00Z2021 Jun2025-04-04T07:52:13.237Z2025-04-04T07:52:13.237ZS-EPMC82855773381813010.1152/physiolgenomics.00114.2020