High impact information on cdc2c

• Therefore, Drosophila cyclin E, which forms a complex with the Dmcdc2c kinase, controls progression through S phase and its down-regulation limits embryonic proliferation [1].
• During Drosophila development and mammalian embryogenesis, exit from the cell cycle is contingent on tightly controlled downregulation of the activity of Cyclin E-Cdk2 complexes that normally promote the transition from G1 to S phase [2].
• Cyclin E-Cdk2 temporally regulates centrosome assembly and establishment of polarity in Caenorhabditis elegans embryos [3].
• Cyclin E-Cdk2 is essential for S phase entry [4].
• We expressed two peptide aptamers, each of which specifically recognizes one of the two essential cyclin-dependent kinases (Cdks), DmCdk1 and DmCdk2, in Drosophila [5].

Biological context of cdc2c

• Distinct modes of cyclin E/cdc2c kinase regulation and S-phase control in mitotic and endoreduplication cycles of Drosophila embryogenesis [6].
• Dup is phosphorylated by cyclin-E/Cdk2, but this direct phosphorylation was not sufficient to explain the rapid destruction of Dup at G1-S [7].
• The Cdk2 mutations in combination with mutant Cdk2 transgenes have allowed us to address the regulatory significance of potential phosphorylation sites in Cdk2 (Thr 18 and Tyr 19) [8].
• The phenotype resulting from mutations in Dmcdc2 was not affected by altering the level of Dmcdc2c [9].
• Reinitiation of DNA replication during the G2 phase of the mitotic cell cycle, therefore, is prevented by cyclin E/Dmcdc2c kinase-independent regulation [6].

Anatomical context of cdc2c

• Here, we suggest a possible mechanism for cyclin E-Cdk2-dependent differentiation: the establishment of cortical polarity by the centrosome [3].

Physical interactions of cdc2c

• Our results reveal that SNR1 helps mediate associations between the Brm complex and DmcycE/CDK2 both in vitro and in vivo [10].
• dacapo encodes a CIP/KIP-type inhibitor of Cyclin E/Cdk2 complexes in Drosophila melanogaster [11].

Other interactions of cdc2c

• In higher eukaryotes, cyclin E is thought to control the progression from G1 into S phase of the cell cycle by associating as a regulatory subunit with cdk2 [8].
• These data suggest that Cyclin D-Cdk4 and Cyclin E-Cdk2 play more versatile roles in Drosophila development [12].
• In Drosophila, the activity of DmcycE/CDK2 is rate limiting for entry into S phase and we previously found that the Brm complex can suppress a reduced growth phenotype associated with a hypomorphic DmcycE mutant [10].
• We have done experiments to investigate a potential functional overlap between two kinases (Dmcdc2 and Dmcdc2c) and two cyclins (cyclin A and cyclin B) [9].
• These results suggest that Drosophila Cdc25 may directly or indirectly increase the kinase activity of Cyclin E-Cdk2 complexes in vivo, thus driving arrested neuroblasts into cell division [13].

References