High impact information on Dp

• ORC localization in Drosophila follicle cells and the effects of mutations in dE2F and dDP [1].
• We screened for mutations that disrupt G1-S transcription late in Drosophila embryogenesis and identified five mutations in the dDP gene [2].
• Elevated expression of dE2F and dDP caused apoptosis in the eye disc [3].
• Ectopic expression of dE2F and dDP induces cell proliferation and death in the Drosophila eye [3].
• In the absence of dDP, the levels of dE2F1 and dE2F2 decline dramatically, and vice versa [4].

Biological context of Dp

• The E2F transcription factor, a heterodimer of E2F and DP subunits, is capable of driving the G1-S transition of the cell cycle [2].
• Although mutations in dDP or dE2F nearly eliminate E2F-dependent G1-S transcription, S-phase still occurs [2].
• Mutation of dDP also causes an incomplete block of DNA replication [5].
• In Drosophila melanogaster the E2f1, E2f2, Dp, and Rbf1 genes all contribute to replication control in ovarian follicle cells, which become 16C polyploid and subsequently undergo chorion gene amplification late in oogenesis [6].
• Mutation of cyclin E prevented the initiation of S phase after overexpression of dE2F/dDP without affecting induction of target gene expression [7].

Anatomical context of Dp

• Mutation of dDP in the germline also prevents nurse cell cytoplasm transfer to the oocyte, resulting in a 'dumpless' phenotype that blocks oocyte development [8].
• In a fraction of the mutant egg chambers the germ cells execute one extra round of mitosis, suggesting that in this tissue dDP is uniquely utilized for cell cycle arrest rather than cell cycle progression [8].

Physical interactions of Dp

• We show that a Drosophila DP protein which can interact co-operatively with E2F proteins is a physiological DNA binding component of Drosophila DRTF1/E2F [9].

Other interactions of Dp

• Mutations in Drosophila DP and E2F distinguish G1-S progression from an associated transcriptional program [2].
• We suggest that dE2F-dDP contributes to the expression of two classes of gene products: replication factors, whose abundance has a graded effect on replication, and cyclin E, which triggers an all-or-nothing transition from G1 to S phase [5].
• These differences correlate with differences in the magnitude of the replication defects in follicle cells, which attain an inappropriate 32C DNA content in both Rbf1 and Dp mutants but not in E2f2 mutants [6].
• Mutation of E2f2, Dp, or Rbf1 causes ectopic DNA replication throughout the follicle cell genome during gene amplification cycles [6].

References