Drosophila melanogaster Cyclin G coordinates cell growth and cell proliferation

Cyclins G1 and G2 are unconventional cyclins whose role in regulating the cell cycle is ambiguous. Cyclin G1 promotes G(2)/M cell cycle arrest in response to DNA damage whereas ectopic expression of CCNG2, which encodes Cyclin G2, induces G(1)/S cell cycle arrest. The only Drosophila Cyclin G was previously shown to be a transcriptional regulator that interacts with the chromatin factor Corto and controls expression of the homeotic gene Abdominal B. It is very close to mammalian Cyclin G1 and G2 except in its N-terminal region, which interacts with Corto and seems to have been acquired in dipterans. Ubiquitous misregulation of Cyclin G (CycG) using transgenic lines lengthens development and induces phenotypes suggesting growth or proliferation defects. Using tissue-specific misregulation of CycG and FACS, we show that overproduction of Cyclin G produces small cells whereas shortage produces large cells, suggesting that Cyclin G negatively regulates cell growth. Furthermore, overexpression of CycG lengthens the cell cycle, with a prominent effect on G(1) and S phases. Genetic interactions with Cyclin E suggest that Cyclin G prevents G(1) to S transition and delays S-phase progression. Control of cell growth and cell cycle by Cylcin G might be achieved via interaction with a network of partners, natably the cyclin-dependent kinases CDK4 and CDK2.