Imprecise excision of the P{EP}EP1614 element, resulting in a deletion of about 500bp removing genomic sequences downstream of the site of the original insertion. The deletion extends towards, but not into, the 5' end of the Lsd-2 GH06230 EST.
Mutant nurse cells show an abnormal pattern of neutral lipid accumulation, beginning at stages 9/10; prominent patches of brightly stained neutral lipids are detected in the cytoplasm of mutant nurse cells, in contrast to the punctuated distribution seen in wild type. The prominent patches often distribute in a radial pattern surrounding the nucleus in the mutant nurse cells. During stages 11/12, neutral lipids aggregate in enlarged lipid structures in the mutant apoptotic nurse cells. Embryos derived from homozygous females contain 50% less triacylglycerol (TAG) than those derived from wild-type females. The level of TAG in homozygous third instar larvae is 27% lower than in wild-type larvae. Embryos derived from homozygous females show a reduced hatching rate of about 63% (this hatching defect is not suppressed by a wild-type paternal copy of Lsd-2). The reduction in viability results from developmental defects occurring after stage 11. No hatching defect is seen in embryos derived from heterozygous females mated to hemizygous males. Lsd-21/Lsd-2KG00149 nurse cells show an abnormal pattern of neutral lipid accumulation.
The 50kD form of Lsd-2 protein is absent in Lsd-21 homozygotes.