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Med24 and Mdh2 are required for Drosophila larval salivary gland cell death
Author(s) -
Wang Lei,
Lam Geanette,
Thummel Carl S.
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22213
Subject(s) - biology , programmed cell death , mediator , microbiology and biotechnology , ecdysone , mutant , mitochondrion , transcription factor , metamorphosis , citric acid cycle , coactivator , gene , genetics , apoptosis , biochemistry , larva , enzyme , ecology
The steroid hormone ecdysone triggers the rapid destruction of larval tissues through transcriptional cascades that culminate in rpr and hid expression and caspase activation. Here, we show that mutations in Mdh2 and Med24 block caspase cleavage and larval salivary gland cell death. Mdh2 encodes a predicted malate dehydrogenase that localizes to mitochondria. Consistent with this proposed function, Mdh2 mutants have significantly lower levels of ATP and accumulate late‐stage citric acid cycle intermediates, suggesting that the cell death defects arise from a deficit in energy production. Med24 encodes a component of the Mediator transcriptional coactivator complex. Unexpectedly, however, expression of the key death regulator genes is normal in Med24 mutant salivary glands. This study identifies novel mechanisms for controlling the destruction of larval tissues during Drosophila metamorphosis and provides new directions for our understanding of steroid‐triggered programmed cell death. Developmental Dynamics 239:954–964, 2010. © 2010 Wiley‐Liss, Inc.