Imprecise excision of P{EP}GE17790 generates an amino-terminal deletion of 340 amino acids in Cul4.
Cul4G1-3 homozygotes exhibit signs of quiescence in the larval brain: neuroblasts show a significant decrease in cell divisions (both DNA replication/EdU staining and Mitosis/phospho-H3); and frequently show a primary cellular process, whereas control neuroblasts show a typically rounded morphology.
Likewise, Cul4G1-3 neuroblast clones in the larval brain also show a significant decrease in cell divisions (DNA replication/EdU staining).
Cul4G1-3 homozygotes on aminoacid-depleted food do not show changes in cell division (DNA replication/EdU staining) on mushroom body neuroblast lineages, as compared to controls.
Homozygous Cul-4G1-3 mutants are arrested in the second-instar larval stage.
When induced between 48-66 hours after egg laying, homozygous mutant Cul-4G1-3 wing disc clones are hardly recovered, indicating a requirement for Cul-4 in cell proliferation or survival. Small Cul-4G1-3 clones, however, are successfully recovered when induced between 66-92 hours after egg laying. These clones are significantly reduced in size compared with wild-type twin clones.
In wild-type twin clones, 13.3% of clone cells label positively for BrdU, whereas in Cul-4G1-3 mutant wing disc clone cells this ratio decreases significantly to 8.8%, indicating that Cul-4 may be required for entry into S phase or for progression of S phase during wing disc development.
During stages 10B-11, whereas there are 32.8% of Cul-4G1-3 mutant cells undergoing apoptosis, 11.6% of display a wild-type BrdU focal pattern and 30.9% mutant cells exhibit reduced or absent BrdU signals. If apoptotic cells are disregarded, about 46% of the surviving cells display reduced BrdU focal patterns, indicating that Cul-4 is required in many follicle cells for BrdU incorporation are focal sites during gene amplification stages. Approximately 24.7% of Cul-4G1-3 mutant cells display ectopic BrdU incorporation. Most mutant cells with weak genomic replication phenotypes also exhibit reduced BrdU signals in chorion foci.
Approximately 27.6% of Cul-4G1-3 mutant follicle cell clones undergo apoptosis.
Cul4[+]/Cul4G1-3 is a suppressor of visible phenotype of Scer\GAL4sca.PU, miGD11624
Cul4[+]/Cul4G1-3 is a suppressor of visible phenotype of Scer\GAL4pnr.PU, miGD11624
Cul4[+]/Cul4G1-3 is a non-suppressor of visible phenotype of Rac2GD17536, Scer\GAL4pnr.PU
Cul4[+]/Cul4G1-3 is a suppressor of macrochaeta phenotype of Scer\GAL4sca.PU, miGD11624
Cul4[+]/Cul4G1-3 is a suppressor of macrochaeta phenotype of Scer\GAL4pnr.PU, miGD11624
Cul4[+]/Cul4G1-3 is a non-suppressor of microchaeta phenotype of Rac2GD17536, Scer\GAL4pnr.PU
Cul4[+]/Cul4G1-3 is a non-suppressor of anterior dorsocentral bristle phenotype of Rac2GD17536, Scer\GAL4pnr.PU
Cul4G1-3 is rescued by Scer\GAL4insc-Mz1407/Cul4UAS.Tag:FLAG
Cul4G1-3 is not rescued by Scer\GAL4insc-Mz1407/Cul4KR.UAS.Tag:FLAG