Imprecise excision of P{EPgy2}desat1EY07679 resulting in the deletion of the first three coding exons and part of the fourth coding exon of desat1.
Homozygosity for allele desat111A and the heteroallelic combination desat111A/desat1119A result in larval lethality with larvae dying during the second larval instar stage (L2), where they remain for up to three days without being able to moult into larval stage three (L3). Very few escapers are able to develop until L3. The mutant larvae are reduced in size and fail to develop beyond L3. The mutant L2 larvae stop feeding and leave the food source.
Clones of homozygous desat111A mutant fat body cells show abnormal autophagic response to starvation.
Ultrastructural analysis reveals that desat111A mutant fat body cells posses fewer autophagic structures (autolysosomes) than wild-type controls. desat111A mutant fat body cells are rich in endoplasmic reticulum and small lysosomes, features that characterise non-starved tissues.
Desat111A is partially rescued by Desat1UAS.cKa/Scer\GAL4ppl.PP