Imprecise excision of P{EP}Atg16G5082, resulting in a 7121bp deletion extending from the original insertion site (revision of data reported in FBrf0235789).
Inferred boundaries of a 7121 bp deletion resulting from the imprecise excision of P{EP}Atg16G5082 that extends from the insertion site into Atg16.
FlyBase curator comment: Authors state that "among our mutants, Atg16d67 is the best to model [inflammatory bowel disease] in flies". "inflammatory bowel disease 10" is associated with human ortholog ATG12L1.
The adult gut of Atg16d67 homozygotes show severe morphological changes, including significant increases in length and diameter, but no changes in the peritrophic membrane thickness, as compared to controls; the epithelium is thicker and shows a significant increase in the proportion of pre-enteroendocrine cel
ls and a reciprocal significant decrease in the proportion of mature enteroendocrine cells, associated with a significant delay in pre-enteroendocrine cell maturation and a significant increase in the overall number of Prospero-positive precursor/mature enteroendocrine cells, but shows no changes in the thickness of the peritrophic membrane, in the proportion of mitotic or apoptotic cells or in cell adhesion, as compared to controls.
Atg16d67 homozygous adults show a severe decrease in lifespan and a significant increase in the gut bacteria burden upon oral infection with Pseudomonas aeruginosa or Enterococcus faecalis, as compared to controls; in the absence of infection, these individuals show a significant increase in the overall gut bacteria burden (namely Lactobacilli and Enterobacteriaceae, but not Acetobacteriaceae), as compared to controls. These mutants do not show significant changes in food uptake.
Starvation-induced formation of acidic autolysosomes (visualized by LysoTracker staining) is blocked in Atg16d67 fat cell somatic clones in mosaic third instar larvae (unlike in the surrounding control cells) as well as in Atg16d67 homozygous larvae.
Atg16d67 mutant adult flies show accumulations of protein aggregates in the brain neurons and display reduced climbing ability in the negative geotaxis assay and shorter lifespan compared to controls.
Atg16d67 has abnormal cell number | adult stage phenotype, suppressible | partially by sliEY10695/Scer\GAL4esg.PU
Atg16d67 has abnormal cell number | adult stage phenotype, suppressible by robo2EP2582/Scer\GAL4esg.PU
Atg16d67 has abnormal immune response | adult stage phenotype, suppressible by sliEY10695/Scer\GAL4esg.PU
Atg16d67 has abnormal immune response | adult stage phenotype, suppressible by robo2EP2582/Scer\GAL4esg.PU
Atg16d67 has adult posterior midgut epithelium phenotype, suppressible | partially by sliEY10695/Scer\GAL4esg.PU
Atg16d67 has enteroendocrine cell | adult stage phenotype, suppressible by sliEY10695/Scer\GAL4esg.PU
Atg16d67 has enteroblast | adult stage phenotype, suppressible | partially by sliEY10695/Scer\GAL4esg.PU
Atg16d67 has adult posterior midgut epithelium phenotype, suppressible by robo2EP2582/Scer\GAL4esg.PU
Atg16d67 has enteroendocrine cell | adult stage phenotype, suppressible by robo2EP2582/Scer\GAL4esg.PU
Atg16d67 has enteroblast | adult stage phenotype, suppressible by robo2EP2582/Scer\GAL4esg.PU
Both the increased proportion of pre-enteroendocrine cells and the reciprocal decreased proportion of mature enteroendocrine cells observed in the adult gut of Atg16d67 homozygotes are fully suppressed by the expression of robo2EP2582 under the control of Scer\GAL4esg.PU, and are fully and partially suppressed, respectively, by the expression of sliEY10695 under the control of Scer\GAL4esg.PU; their severely decreased lifespan upon oral infection with Pseudomonas aeruginosa or Enterococcus faecalis is also suppressed by the expression of sliEY10695 or robo2EP2582 under the control of Scer\GAL4esg.PU.
Atg16d67 is rescued by Atg16UAS.c.Tag:FLAG/Scer\GAL4esg.PU
Atg16d67 is rescued by Atg16ΔAutD.UAS/Scer\GAL4esg.PU
Atg16d67 is rescued by Atg16ΔAutD+Linker.UAS/Scer\GAL4esg.PU
Atg16d67 is rescued by Atg16Tag:HA
Atg16d67 is not rescued by Atg16ΔWD40.UAS/Scer\GAL4esg.PU
Both the increased proportion of pre-enteroendocrine cells and the reciprocal decreased proportion of mature enteroendocrine cells observed in the adult gut of Atg16d67 homozygotes are fully suppressed by the expression of Atg16Scer\UAS.c.T:Zzzz\FLAG, Atg16ΔAutD.Scer\UAS or Atg16ΔAutD+Linker.Scer\UAS, but not Atg16ΔWD40.Scer\UAS, under the control of Scer\GAL4esg.PU.
The severely decreased lifespan of Atg16d67 homozygotes upon oral infection with Pseudomonas aeruginosa or Enterococcus faecalis is suppressed by the expression of Atg16ΔAutD+Linker.Scer\UAS, but not Atg16ΔWD40.Scer\UAS, under the control of Scer\GAL4esg.PU.
The abrogated formation of acidic lysosomes in fat body cells in Atg16d67 homozygous third instar larvae as well as the accumulation of protein aggregates in brain neurons in adult flies, their reduced climbing ability and shorter lifespan can be rescued by combination with Atg16T:Ivir\HA1.