The lipid storage droplet-2 (LSD-2) protein of Drosophila is a homolog of mammalian perilipin 2,
which is essential for promoting lipid accumulation and lipid droplet formation. The function of
LSD-2 as a regulator of lipolysis has also been demonstrated. However, other LSD-2 functions remain
unclear. To investigate the role of LSD-2, we performed tissue-specific depletion in the salivary
glands of Drosophila using a combination of the Gal4-upstream activating sequence system and RNA
interference. LSD-2 depletion inhibited the entry of salivary gland cells into the endoreplication cycle
and delayed this process by enhancing CycE expression, disrupting the development of this organ. The
deficiency of LSD-2 expression enhanced reactive oxygen species production in the salivary gland and
promoted JNK-dependent apoptosis by suppressing dMyc expression. This phenomenon did not result
from lipolysis. Therefore, LSD-2 is vital for endoreplication cell cycle and cell death programs.