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Published November 1996 | Published
Journal Article Open

A maternal requirement for glutamine synthetase I for the mitotic cycles of syncytial Drosophila embryos

Abstract

We describe the maternal effect phenotype of a hypomorphic mutation in the Drosophila gene for glutamine synthetase I (GSI). The extent of development of embryos derived from homozygous mutant females is variable, although most mutant embryos fail to survive past germband elongation and none develop into larvae. These embryos are characterised by an increase in the number of yolk-like nuclei following nuclear migration to the cortex. These nuclei appear to fall into the interior of the embryo from the cortex at blastoderm. As they do so, the majority continue to show association with PCNA in synchrony with nuclei at the cortex, suggesting some continuity of the synchrony of DNA replication. However, the occurrence of nuclei that have lost cell cycle synchrony with their neighbours is not uncommon. Immunostaining of mutant embryos revealed a range of mitotic defects, ultimately resulting in nuclear fusion events, division failure or other mitotic abnormalities. A high proportion of these mitotic figures show chromatin bridging at anaphase and telophase consistent with progression through mitosis in the presence of incompletely replicated DNA. GSI is responsible for the ATP-dependent amination of glutamate to produce glutamine, which is required in the formation of amino acids, purines and pyrimidines. We discuss how the loss of glutamine could depress both protein and DNA synthesis and lead to a variety of mitotic defects in this embryonic system that lacks certain checkpoint controls.

Additional Information

© 1996 by Company of Biologists. (Received 8 May 1996 - Accepted 22 July 1996) This work was supported by grants from the Cancer Research Campaign. L.M.F. was the holder of a Research Studentship from the Science and Engineering Research Council (SERC). We thank Fay Shamanski and Terry Orr-Weaver for communicating to us their unpublished data on throng, and providing us with this mutant. We acknowledge helpful discussion from many of our colleagues during the course of this work, and the helpful comments of Emma Warbrick on the manuscript.

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