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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Atg16l1tm1Aki
targeted mutation 1, Shizuo Akira
MGI:3818483
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Atg16l1tm1Aki/Atg16l1tm1Aki involves: 129/Sv * C57BL/6 MGI:3818489


Genotype
MGI:3818489
hm1
Allelic
Composition
Atg16l1tm1Aki/Atg16l1tm1Aki
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg16l1tm1Aki mutation (0 available); any Atg16l1 mutation (44 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• mouse embryonic fibroblasts (MEFs) fail to form autophagosomes when deprived of nutrients
• MEFs fail to form autophagosomes when deprived of nutrients
• degradation of long lived proteins in MEFs is reduced by about a third

mortality/aging
• neonates die within one day of delivery due to an inability to survive neonatal starvation

cellular
• mouse embryonic fibroblasts (MEFs) fail to form autophagosomes when deprived of nutrients
• MEFs fail to form autophagosomes when deprived of nutrients
• degradation of long lived proteins in MEFs is reduced by about a third

immune system
• irradiated wild-type mice that have received mutant fetal liver cells to replace all haematopoietic cells are highly susceptible to dextran sulfate sodium (DSS)-induced colitis
• five days after DSS treatment, all mice die of an inflammatory bowel disease compared to controls that all live
• severe inflammation in the colon results from the DSS treatment with larger areas of ulceration and increased infiltration of lymphocytes
• body weight loss is more severe with mice losing 25% of their bodyweight before dying
• levels of IL-1beta and IL-18 are elevated in the sera of mice with 4 days of DSS treatment
• IL-1beta production by fetal-derived or chimeric-derived macrophages is enhanced to TLR3, TLR4, TLR7 and TLR9 ligands
• levels of reactive oxygen species is higher in fetal liver-derived macrophages than controls after stimulation with LPS
• IL-1beta production by fetal-derived macrophages is highly elevated (6-10 fold) when stimulated with LPS or synthetic lipid A
• similar results are obtained from peritoneal or bone-marrow derived macrophages that are isolated from irradiated mice that have received mutant fetal liver cells
• higher augmentation of IL-1beta production by fetal-derived macrophages occurs with incubation of several different species of non-invasive Gram-negative bacteria
• IL-1beta production by fetal-derived macrophages is enhanced to a lesser degree by ligands for TLR3, TLR7 and TLR9
• IL-18 secretion is enhanced in fetal-derived macrophages when stimulated with LPS

digestive/alimentary system
• irradiated wild-type mice that have received mutant fetal liver cells to replace all haematopoietic cells are highly susceptible to dextran sulfate sodium (DSS)-induced colitis
• five days after DSS treatment, all mice die of an inflammatory bowel disease compared to controls that all live
• severe inflammation in the colon results from the DSS treatment with larger areas of ulceration and increased infiltration of lymphocytes
• body weight loss is more severe with mice losing 25% of their bodyweight before dying
• levels of IL-1beta and IL-18 are elevated in the sera of mice with 4 days of DSS treatment

hematopoietic system
• IL-1beta production by fetal-derived or chimeric-derived macrophages is enhanced to TLR3, TLR4, TLR7 and TLR9 ligands
• levels of reactive oxygen species is higher in fetal liver-derived macrophages than controls after stimulation with LPS





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
03/12/2024
MGI 6.23
The Jackson Laboratory