Mutants die before the mid-pupal stage.
Embryos lacking both maternal and zygotic SNF1A+ function (derived from homozygous female germline clones) do not develop into larvae. The mutant embryos have severely deformed cuticle structures and ventral denticle belts are missing. Ultrastructurally, the surface of the embryo is roughened and the columnar structure of the epidermis is disorganised. Some cells contain abnormally enlarged nuclei in these embryos, and approximately 30% of mitotic cells are polyploid.
Homozygous larvae have a high fraction of mitotic brain neuroblasts that show extreme polyploidy.
AMPKαD1 has abnormal mitotic cell cycle | larval stage phenotype, suppressible | partially by sqhE20.E21
AMPKαD1 has abnormal mitotic cell cycle | larval stage phenotype, non-suppressible by Lkb1UAS.cLa/Scer\GAL4hs.PB
AMPKαD1 has embryonic/first instar larval cuticle | maternal effect phenotype, suppressible | partially by sqhE20.E21
The cuticle defects seen in mutant embryos derived from SNF1AD1 homozygous female germline clones are partially suppressed by sqhE20.E21; the fraction of embryos that form cuticle is increased from approximately 10% to approximately 30%.
The fraction of SNF1AD1 mitotic larval brain neuroblasts that show extreme polyploidy is decreased if the larvae are also mutant for sqhE20.E21.
The fraction of SNF1AD1 mitotic larval brain neuroblasts that show extreme polyploidy is not changed if the larvae are also co-expressing lkb1Scer\UAS.cLa under the control of Scer\GAL4hs.PB.
AMPKαD1 is rescued by AMPKαWT.UAS/Scer\GAL4Tub.PU
AMPKαD1 is not rescued by AMPKαKR.UAS/Scer\GAL4Tub.PU