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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

2.6kb deletion.

2.6kb deletion breaks in the ncd transcription unit, removing its 5' section, and extends into ca.

Caused by aberration
Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

meiosis & nuclear chromosome

meiosis & nuclear chromosome & oocyte

meiosis & nuclear chromosome | female (with ncdD)

meiosis II & spindle & egg

mitosis & nuclear chromosome

mitotic anaphase & spindle

mitotic metaphase & spindle

Detailed Description

During meiosis in the oocyte and mitosis in the early embryo, ncd1 mutants show frequent chromosome mis-segregation, with elevated levels of chromosome nondisjunction and loss.

18% of ncd1/ncd1 mutant brains display disorganised metaphase compared to 11% in wild-type brains. 55% of brains show lagging chromosomes at anaphase compared to 9% in wild-type brains.

Throughout cycles 11, 12 and 13, spindle pole-to-furrow distances are indistinguishable when comparing wild-type and ncd1 embryos. The separation rate of the spindle poles differs by 28% between wild-type and ncd1 cycle 13.

ncd1 females have disorganised meiotic spindles in the oocyte.

The nuclear lamina in ncd1 mutant larval stage brains is similar to that of wild type.

The rate of microtubule flux during metaphase A and anaphase in ncd1 embryos is 0.041 +/- 0.021 μm/s, which is not significantly different from the value of 0.032 +/- 0.13 in wild-type embryos. During anaphase B, microtubule flux decreases to about zero in mutant embryos, as occurs in wild-type embryos. The persistence of the prometaphase and the metaphase/anaphase A isometric states is decreased significantly in ncd1 embryos.

ncd1/ncdD females show 32% X chromosome nondisjunction and 48% 4th chromosome nondisjunction.

The overall rate and extent of spindle pole separation is much greater than in wild-type embryos. The early fast phase of spindle pole separation occurs at roughly the same rate as in wild-type embryos, but overshoots. This results in an overall decrease in the length of each mitotic cycle. Interzonal microtubules are disorganised in many spindles. The rate of spindle pole migration is rescued to wild type by injection of antibodies against dynein heavy chain.

Most of the meiotic exceptions result from chromosome loss. Frayed and monopolar spindles are frequently observed.

In contrast to the situation in wild-type embryos, the inhibition of Klp61F function (via injected antibodies) in ncd1 embryos does not inhibit the formation of bipolar metaphase spindles. Spindles form and do not collapse but successfully complete anaphase A, appear relatively normal during anaphase B with marked defects only appearing in the later stages of anaphase B and telophase.

Meiosis II spindles of homozygous eggs are highly abnormal. Depolymerising microtubules are seen in the region of the spindle where the central spindle body forms in wild-type eggs. The distal ends of the spindle are split into 2 or 3 poles, and spindle spurs associated with partially detached chromosomes are sometimes seen. Approximately 90% of eggs laid by homozygous females fail to hatch.

Transmission rate of Dp(1;f)J21A through females to progeny is 28%, the ncd mutation strongly decreases transmission. Mutation also decreases transmission of Dp(1;f)1B, Dp(1;f)25A and Dp(1;f)10B.

Homozygous females show increased meiotic and mitotic chromosome segregation compared to wild-type. Embryos derived from homozygous females have reduced viability.

Mutants exhibit mitotic chromosome mis-segregation.

Oocytes display a wide range of abnormal spindle configurations. The process of spindle pole assembly is dramatically affected. In addition the spindle is unstable and degenerates to form an apolar or multipolar array, then reforms a relatively normal bipolar organisation and then degenerates again. Spindle instability may explain much of the cytological variability. After nuclear envelope breakdown the karyosome and associated microtubules moves through the ooplasm.

The frequency of X chromosome disjunction is 0.381 and the frequency of chromosome 4 segregation is 0.604 in homozygotes. Embryos derived from ncd1/ncd1 ncdMC2/ncdMC2 females have curved or bent spindles and split centrosomes at one or both spindle poles.

Axsr2/+ ncd1/+ females show much higher levels of both X and fourth chromosomal non-disjunction than do either of the single heterozygotes.

Meiotic divisions in homozygous oocytes are abnormal. In metaphase I, spindles may appear incomplete, frayed or broad and diffuse, and abnormal chromosome movements and mislocalised chromosomes are seen. Anaphase I meiotic figures usually appear abnormal, with chromosomes oriented along parallel, but widely separated axes of division, or on multiple axes of division. The chromosomes typically appear widely scattered. Telophase II nuclei vary in number and size. Polar bodies are not seen in early embryos, instead spindle-associated chromosomes are often observed in the anterodorsal region of the embryo where the polar bodies are normally found. Normally fertilised early embryos show unusual metaphase and anaphase cleavage spindles with frayed mid-regions, secondary spindle branches, or abnormally wide or distorted regions.

Affects meiotic segregation of all chromosomes in females.

ncd1/ncd7 females produce a high frequency of non-disjunctional exceptions and mosaics, including gynandromorphs, among their offspring.

A high frequency of gynandromorphs are produced, due to mitotic loss of X chromosomes. There is a strong preference for the loss of maternally derived X chromosomes, although paternally derived X chromosomes can be lost. There is also a higher than normal frequency of meiotic nondisjunction and chromosome loss.

ncd7/ncd1 females produce a high frequency (27.7%) of non-disjunctional exceptions and mosaics, including gynandromorphs, among their offspring. Non-disjunction of the X chromosome and chromosome 4 occurs at meiosis I.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by

ncd1 has abnormal meiotic cell cycle phenotype, non-enhanceable by sub[+]/sub1794

Suppressed by
Enhancer of
NOT Enhancer of

ncd[+]/ncd1 is a non-enhancer of abnormal meiotic cell cycle phenotype of sub1794

Suppressor of
Phenotype Manifest In
Suppressed by

ncdD/ncd1 has meiosis & nuclear chromosome | female phenotype, suppressible by lwr05486/lwr[+]

Enhancer of

ncd1 is an enhancer of phenotype of noda

ncd1 is an enhancer of phenotype of nod4

ncd1 is an enhancer of phenotype of nod3

ncd1 is an enhancer of phenotype of nod2

ncd1 is an enhancer of phenotype of nod6

NOT Enhancer of

ncd1/ncd1 is a non-enhancer of spindle phenotype of sub1794

Suppressor of

ncd1/ncd1 is a suppressor of brain | larval stage phenotype of sub131/sub1

ncd1 is a suppressor of aster & neuroblast & larva phenotype of Klp61Furc-1

ncd1 is a suppressor of spindle & neuroblast & larva phenotype of Klp61Furc-1

ncd1 is a suppressor of spindle & neuroblast & larva phenotype of Klp61F07012


Klp61F07012/Df(3L)bab-PG, ncd1 has nuclear lamina & neuroblast & larva phenotype

Klp61F06345, ncd1 has chromatin & spermatocyte phenotype

Klp61Furc-1, ncd1 has nuclear lamina & neuroblast & larva phenotype

Klp61Furc-1/Klp61F07012, ncd1 has nuclear lamina & neuroblast & larva phenotype

Additional Comments
Genetic Interactions

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.

balltrip ncd1 double mutants exhibit a mixture of the ncd1 and balltrip phenotypes, namely, multiple spindles and unfocused poles.

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.

ncd1/ncdD female X and 4th chromosome nondisjunction is dominantly suppressed by lwr05486.

The ncd1 inviability is dominantly enhanced by γTub37C13 or γTub37C12; ncd1 females heterozygous for γTub37C13 or γTub37C12 lay eggs but more than 99% fail to hatch.

ncd1 acts as a dominant enhancer of the nod locus; ncd1 heterozygous females also heterozygous for noda, nod6, nod4, nod3, nod2 or Df(1)nod show an increased level of X and fourth chromosome nondisjunction.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

ncd1 is partially rescued by ncdGFP

ncd1 is partially rescued by ncd2.GFP(S65T)

ncd1 is partially rescued by ncdGFP(S65T)

ncd1 is partially rescued by ncdMC2

Not rescued by

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.

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Stocks (6)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (44)