A number of mutations have been introduced into Npc1b; a stop codon at amino acid position 392, several splice-site mutations and an XhoI diagnostic restriction site.
Depletion of apical membrane sterol in the gut is more dramatic in Npc1b1 mutants compared to wild-type larvae when fed with lipid-depleted medium.
Hemizygous and homozygous mutants die at the second instar larval stage. The mutant larvae show no gross morphological or behavioural defects and are able to survive for at least a week as second instar larvae. Approximately 5% of the mutant larvae arrest at the moult from second to third instar.
Npc1b1/Npc1bR9-28 animals die at the second instar larval stage and are able to survive for at least a week as second instar larvae.
The ratio of absorbed cholesterol:glucose is severely reduced in Npc1b1 first instar larvae relative to wild type.
The midgut tissues of mutant larvae appear to be largely devoid of filipin staining (a fluorescent cholesterol-binding compound) relative to wild type and do not display any accumulation of sterol-rich trafficking organelles.
Npc1b1 is rescued by Npc1b+t6.6
Npc1b1 is rescued by Npc1bUASp.cVa/Scer\GAL4Npc1b.PV
