Myo61F920 mutant larvae (Df(3L)920 animals in which mtacp1 function has been rescued using mtacp1Ubi.PH) show no differences in either gut pH regulation or food clearance rates compared to controls. However, the mutant midgut contains a greater number of apoptotic nuclei than in the control gut, with the increase apoptotic nuclei being seen in the gastric caecum, anterior midgut and the copper cell region. These apoptotic cells are enterocytes.
Myo61F920 mutant larvae have defects in the ultrastructure of the brush border of the midgut. Many defects are seen in the midgut epithelium, including microvillus vesiculation, membrane-tethering defects and a general disorganised appearance. The enterocytes of the anterior midgut generally have the most severe brush border defects, whereas defects are less severe to absent in the posterior midgut.
Homogenates from Myo61F920 mutant larval midgut preparations (isolated under hypotonic conditions) contain far fewer isolated brush borders than homogenates from wild-type larvae. Those fragments that are derived from the brush border are less densely packed and more irregular in length in homogenates from mutant larvae and they are characterised by membrane sloughing from the underlying actin cytoskeleton. Ultrastructurally, the mutant brush border preparations lack the lateral tethers than normally link the microvillus core to the membrane and the central actin bundles of the microvillus are less densely packed than normal, with some of the actin filaments resting against the outer membrane (instead of being tightly packed in the centre of the microvillus).
Myo61F920 mutant larvae are hypersensitive to oral infection by P.entomophila compared to control larvae. Infected mutant larvae have severe brush border defects in the proximal midgut as early as 2 hours after infection (in contrast to control larvae which have near normal brush border morphology at this time).
Myo61F920 is rescued by Myo61F+t5.7