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First published online October 22, 2003

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Modelling oxidative-stress-induced apoptosis in flies

Reactive oxygen species (ROS), by-products of aerobic metabolism, can severely damage DNA, protein and lipids and cause apoptosis if allowed to accumulate within cells. Selenoproteins are important ROS scavengers in many species, and on p. 4597 Florenci Serras and co-workers provide more details about the link between selenoproteins, ROS accumulation and cell death. They describe how ROS-induced apoptosis in Drosophila imaginal disc cells carrying a selD^ptuf mutation, which impairs selenoprotein synthesis, is driven mainly by the caspase-dependent Dmp53/Rpr pathway. The researchers show that the apoptotic effect of selD^ptuf, a recessive null mutation in the Drosophila homologue of human selenophosphate synthetase type 1 (sps1), does not require the activity of head involution defective (hid), a potent activator of caspase-dependent apoptosis. Instead, stabilisation of the Drosophila homologue of the p53 tumour suppressor, Dmp53, in selD^ptuf mutant cells results in transcription of the pro-apoptotic gene reaper (rpr), activation of the initiator caspase DRONC, processing of the effector caspase DRICE, and ultimately death of the selD^ptuf mutant cells. Moreover, ectopic expression of DIAPI, an inhibitor of apoptosis that directly inhibits caspases, rescues selD^ptuf cells from death.

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Related articles in JCS:

DIAP1 suppresses ROS-induced apoptosis caused by impairment of the selD/sps1 homolog in Drosophila

Marta Morey, Montserrat Corominas, and Florenci Serras
JCS 2003 116: 4597-4604. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?