Amino acid replacement: Q102term.
C13485994T
Q102term | cid-PA
Q102term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
cidT11-2/cidT22-4 mutant embryos die around stage 15 of embryogenesis, and display a phenotypic series that correlates with the temporal disappearence of maternal cid protein and the absence of newly synthesised zygotic protein. At embryonic stages 9-10, cidT11-2/cidT22-4 mutant embryos display lagging chromosomes during anaphase and unresolved chromatin bridges during telophase, which are not observed in heterozygous controls.
Later stage cidT11-2/cidT22-4 mutant embryos display a high degree of disorganization of the developing nervous tissue, with obvious micronuclei, large presumably polyploid nuclei, very few true metaphase plates, and few anaphases and telophases. The overall nuclear density is much lower in cidT11-2/cidT22-4 embryos than wild-type, consistent with the aneuploidy that results from failures in chromosome segregation and cell division.
cidT11-2/cidT22-4 mutants display a 2.4-fold higher mitotic index and a 2-fold higher number of cells positive for CycA and CycB, in comparison with wild-type controls. cidT11-2/cidT22-4 mutants show a marked increase in the number of cells in prophase and prometaphase, as judged by chromosome and spinlde morphology. Very few cells progress to anaphase in cidT11-2/cidT22-4 mutants, suggesting that they are delayed prior to the metaphase-anaphase transition.
Treatment of cidT11-2/cidT22-4 mutants with doxorubicin (which generates dsDNA breaks) has little effect on the mitotic index of these mutants, indicating that these cells are already delayed in mitosis at the time of drug addition (heterozygotes exhibit dramatically decreased mitotic indexes upon addition).
Inactivation of mei-41 by caffeine treatment does not suppress cidT11-2/cidT22-4-mediated mitotic delay. The mitotic index of cidT11-2/cidT22-4 mutants remains nearly twice that of heterozygous controls and most of the mitotic cells are found in prophase or prometaphase, with very few cells progressing to later stages of mitosis.
Both homozygous and heterozygous cidT11-2/cidT22-4 mutant cells are delayed in response to colcemid treatment. They display a nearly 2-fold increase in mitotic index after 1 hour of treatment, accompanied by a large increase in the number of cells accumulated in prometaphase.
cidT11-2/cidT22-4 has abnormal cell cycle phenotype, suppressible | partially by BubR1k03113
cidT11-2/cidT22-4 has abnormal mitotic cell cycle | embryonic stage phenotype, suppressible | partially by BubR1k03113
The presence of a BubR1k03113 mutant background suppresses the increased mitotic index phenotype associated with cidT11-2/cidT22-4 mutants. The number of cells delayed in prophase and prometaphase also decreases dramatically in double mutants, whereas the number of cells in anaphase shows a corresponding increase and is greater than controls. BubR1k03113 cidT11-2/cidT22-4 double mutants exhibit a mitotic index nearly double that of cidT11-2/cidT22-4 single mutants.
When provided by the mother, a single copy of cidT:Avic\GFP-EGFP (insertion line III.2) rescues the lethality of cidT12-1/cidT22-4 transheterozygotes with high efficiency (88% of expected).
