Morphological irregularities and features of resistance to apoptosis in the dcp-1/pita double mutated egg chambers during Drosophila oogenesis.
In the present study, we demonstrate the most novel characteristic morphological features of Drosophila egg chambers lacking both dcp-1 and pita functions in the germline cells. Dcp-1 is an effector caspase and it has been previously shown to play an important role during Drosophila oogenesis [McCall and Steller, 1998 : Science 279 : 230-234; Laundrie et al., 2003 : Genetics 165 : 1881-1888; Peterson et al., 2003 : Dev Biol 260 : 113-123]. The completion of sequencing and annotation of the Drosophila genome has revealed that the dcp-1 gene is nested within an intron of another distinct gene, called pita, a member of the C2H2 zinc finger protein family that regulates transcriptional initiation. The dcp-1(-/-)/pita(-/-) nurse cells exhibit euchromatic nuclei (delay of apoptosis) during the late stages of oogenesis, as revealed by conventional light and electron microscopy. The phalloidin-FITC staining discloses significant defects in actin cytoskeleton arrangement. The actin bundles fail to organize properly and the distribution of actin filaments in the ring canals is changed compared to the wild type. The oocyte and the chorion structures have been also modified. The oocyte nucleus is out of position and the chorion appears to contain irregular foldings, while the respiratory filaments obtain an altered morphology. The dcp-1(-/-)/pita(-/-) egg chambers do not exhibit the rare events of spontaneously induced apoptosis, observed for the wild type flies, during mid-oogenesis. Interestingly, the mutated egg chambers are protected by staurosporine-induced apoptosis in a percentage of 40%, strongly suggesting the essential role of dcp-1 and/or pita during mid-oogenesis.
Nezis
Ioannis P
IP
Faculty of Biology, Department of Cell Biology and Biophysics, University of Athens, Athens, Greece.
Stravopodis
Dimitrios J
DJ
Papassideri
Issidora S
IS
Stergiopoulos
Costas
C
Margaritis
Lukas H
LH
D000199:Actins / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D030801:Animals, Genetically Modified; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics*; D020169:Caspases / Q000172:deficiency / Q000235:genetics*; D003599:Cytoskeleton / Q000378:metabolism / Q000648:ultrastructure; D004330:Drosophila / Q000235:genetics / Q000502:physiology*; D029721:Drosophila Proteins / Q000172:deficiency / Q000235:genetics*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005047:Etoposide / Q000494:pharmacology; D005260:Female; D018613:Microscopy, Confocal; D009154:Mutation; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D009865:Oocytes / Q000378:metabolism / Q000648:ultrastructure; D009866:Oogenesis / Q000502:physiology*; D010053:Ovary / Q000166:cytology / Q000201:enzymology; D019311:Staurosporine / Q000494:pharmacology
D000199:Actins; D029721:Drosophila Proteins; D004791:Enzyme Inhibitors; D019384:Nucleic Acid Synthesis Inhibitors; D005047:Etoposide; D020169:Caspases; C103568:Dcp-1 protein, Drosophila; D019311:Staurosporine