Vps16B1 homozygous adults show significant decrease in lifespan upon infection with heat-killed E.coli bacteria, as compared to infected controls.
Vps16B1 flies exhibit a profound defect in phagosome maturation, and as a consequence are sensitive to infections with normally non-pathogenic microbes. Vps16B1mutants are strongly susceptible to infections with Escherichia coli (that are not normally pathogenic to flies).
Pathogenic Enterococcus faecalis microbes kill Vps16B1 flies only slightly faster than wild-type.
Vps16B1 hemocytes do not exhibit a defect in initial phagocytic uptake of bacteria. After 45 minutes however, Vps16B1 mutant hemocytes are full of bacteria and do not seem able to digest them. The bacterial burden remains elevated, as opposed to the efficient clearance of the majority of bacteria in wild-type flies after just 1 day.
Vps16B1 phagosomes fail to acidify.
Eyes of two-day old Vps16B1 mutants exhibit normal ommatidial organization.
Starvation-induced autophagy, which requires fusion with lysosomes, is normal in Vps16B1 larvae.
Vps16B1 flies exhibit normal lysosomal function.
Vps16B1 flies do not show any morphological defects.