meiosis & nuclear chromosome
meiosis & nuclear chromosome & oocyte
meiosis II & spindle & egg
mitosis & nuclear chromosome
mitotic anaphase & spindle
mitotic metaphase & spindle
The early cleavage defects seen in embryos derived from αTub67Ckav-21g/+ females are partially suppressed by ncd1/+, with the embryos reaching a later stage of development (43.3% of 3-4 hour embryos derived from the double heterozygous females resemble a normal cellular blastoderm).
ncd1 enhances the developmental rate defects seen in flies expressing SAKUbi.T:Avic\GFP, although the flies that hatch are all morphologically normal. A dramatic increase is seen in the rate of spindle multipolarity during prophase and metaphase, but as in SAKUbi.T:Avic\GFP alone, no multipolar spindles are seen during anaphase. Polyploidy, aneuploidy and lagging chromosomes are all seen during anaphase. The mitotic index is higher than in flies expressing SAKUbi.T:Avic\GFP alone.
Klp61F06345 ncd9/Klp61Furc-1 ncd1 adults are recovered at 28% of the frequency expected for full viability. Biastral spindles are not found in Klp61Furc-1 mutants, but comprise more than 66% of spindles in Klp61Furc-1 ncd1 mutants. More than 96% of Klp61F07012 ncd1 double mutant spindles are biastral. Klp61Furc-1 ncd1 double mutants survive longer as third instar larvae and show increased cell proliferation in comparison to Klp61Furc-1 mutants. The nuclear lamina in interphase cells of Klp61Furc-1 ncd1/Klp61F07012 ncd1 double mutant larval stage brains is indistinguishable from that of wild type. However, in most mitotic double mutant cells, a nuclear lamina can not be detected or is very disorganised (in contrast to wild type). Klp61F07012/Df(3L)bab-PG ncd1 cells have a monopolar organisation of chromosomes and centrosomes, showing nuclear lamina involutions that extend towards centrally located centrosomes. Klp61F07012 ncd1/Klp61Furc-1 ncd1 cells have a monopolar organisation of chromosomes and centrosomes, showing nuclear lamina involutions that extend towards centrally located centrosomes. A number of spermatocytes of Klp61F07012 ncd1 mutants and mutants homozygous for ncd1 but transheterozygous for Klp61F07012/Klp61Furc-1 exhibit several small nuclei at the poles of telophase spindles and some post-meiotic spermatids also contained micronuclei. Biastral spindles in Klp61F06345 ncd1 spermatocytes sometimes show multiple masses of γ-tubulin at spindle poles and an apparently polyploid complement of chromatin.
sub1794 show allele specific interactions with alleles of ncd. sub1794/+, ncdD/+ transheterozygotes show a high frequency of non-disjunction, whereas either mutation alone is completely recessive. sub1794/+, ncd1/+ transheterozygotes do not show this effect. Double mutants of sub1794 with ncd1 show no greater degree of oocyte spindle pole abnormality that those of ncd1 mutants alone - the effects of the two mutants are simply additive.
The chromosome segregation phenotype is almost completely rescued by ncdT:Avic\GFP, and the embryo viability phenotype is partially rescued by two copies of ncdT:Avic\GFP. Both phenotypes appear to completely rescued by four copies of ncdT:Avic\GFP. Two copies of ncdT:Avic\GFP-S65T partially rescue the ncd1 phenotype, while four copies of ncdT:Avic\GFP-S65T essentially completely rescue the ncd1 phenotype.
Chromosome segregation and embryo viability can be rescued by 4 copies of ncdT:Avic\GFP-S65T, 2 copies gives only partial rescue. Chromosome segregation and embryo viability can also be rescued by 4 copies of ncdT:Avic\GFP, 2 copies gives only partial rescue. ncd2.T:Avic\GFP-S65T fails to rescue both aspects of the phenotype.
The disjunction phenotype is partially rescued to a frequency of 0.237 for the X chromosome and 0.152 for chromosome 4 by one copy of ncdMC2. Viability is also improved by ncdMC2. Rescue of non-disjunction of the X chromosome and viability, but not non-disjunction of chromosome 4 is dosage sensitive, increasing with two copies of ncdMC2. ncd+mEa fully rescues the ncd1 phenotype.