After DNA damage, many cells appear to enter a sustained arrest in the G 2 phase of the cell cycle. It is shown here that this arrest could be sustained only when p53 was present in the cell and capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21. After disruption of either the p53 or the p21 gene, γ radiated cells progressed into mitosis and exhibited a G 2 DNA content only because of a failure of cytokinesis. Thus, p53 and p21 appear to be essential for maintaining the G 2 checkpoint in human cells.

https://science.sciencemag.org/content/sci/282/5393/1497.full.pdf

Requirement for p53 and p21 to Sustain G2 Arrest After DNA Damage

Autonomous Control of Cell and Organ Size by CHICO, a Drosophila Homolog of Vertebrate IRS1–4

A fundamental goal of genetics and functional genomics is to identify and mutate every gene in model organisms such as Drosophila melanogaster. The Berkeley Drosophila Genome Project (BDGP) gene disruption project generates single P-element insertion strains that each mutate unique genomic open reading frames. Such strains strongly facilitate further genetic and molecular studies of the disrupted loci, but it has remained unclear if P elements can be used to mutate all Drosophila genes. We now report that the primary collection has grown to contain 1045 strains that disrupt more than 25% of the estimated 3600 Drosophila genes that are essential for adult viability. Of these P insertions, 67% have been verified by genetic tests to cause the associated recessive mutant phenotypes, and the validity of most of the remaining lines is predicted on statistical grounds. Sequences flanking >920 insertions have been determined to exactly position them in the genome and to identify 376 potentially affected transcripts from collections of EST sequences. Strains in the BDGP collection are available from the Bloomington Stock Center and have already assisted the research community in characterizing >250 Drosophila genes. The likely identity of 131 additional genes in the collection is reported here. Our results show that Drosophila genes have a wide range of sensitivity to inactivation by P elements, and provide a rationale for greatly expanding the BDGP primary collection based entirely on insertion site sequencing. We predict that this approach can bring >85% of all Drosophila open reading frames under experimental control.

https://www.genetics.org/content/genetics/153/1/135.full.pdf

The Berkeley Drosophila Genome Project gene disruption project: Single P-element insertions mutating 25% of vital Drosophila genes.

Endoreplication cell cycles: more for less.

https://www.cell.com/current-biology/pdf/S0960-9822(98)70089-2.pdf

Fluctuations in cyclin e levels are required for multiple rounds of endocycle s phase in drosophila

The yeast MCM2, MCM3, and MCM5/CDC46 genes are required for DNA replication and have been proposed to act as factors that license the DNA for one and only one round of replication per cell cycle. We have identified a Drosophila gene, DmMCM2, that is highly homologous to MCM2. A P-element insertion into this gene, which prevents its transcription, inhibits proliferation of cells in the imaginal discs and central nervous system (CNS) and causes an apparent prolongation of S phase in the embryonic and larval CNS. DmMCM2 is expressed in the embryo in a pattern corresponding to that of S-phase cells. These results suggest that DmMCM2 plays a role in the regulation of DNA replication analogous to that of its yeast counterpart.

Peter Follette

Papers

Fluctuations in cyclin e levels are required for multiple rounds of endocycle s phase in drosophila

Cell proliferation and DNA replication defects in a Drosophila MCM2 mutant.

Qualifying for the license to replicate.

Cdks and the Drosophila cell cycle.

Connecting cell behavior to patterning: lessons from the cell cycle.