FlyBase Allele Report: Dmel\ncd[1]

General Information

Symbol

Dmel\ncd¹

Species

D. melanogaster

Name

FlyBase ID

FBal0012910

Feature type

allele

Associated gene

Dmel\ncd

Associated Insertion(s)

Carried in Construct

Also Known As

ca^nd

Key Links

Allele class

loss of function allele

Mutagen

X ray

Nature of the Allele

Allele class

loss of function allele

(Komma and Endow, 1997, Endow and Komma, 1996, Endow et al., 1994, Hatsumi and Endow, 1992, Endow et al., 1990)

Mutagen

X ray

(Endow and Komma, 1997)

Progenitor genotype

Caused by aberration

Df(3R)ca^nd1

Cytology

Description

2.6kb deletion.

(Knowles and Hawley, 1991)

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

(Yamamoto et al., 1989)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal meiotic cell cycle

(Hatsumi and Endow, 1992, Komma et al., 1991, Sequeira et al., 1989)

abnormal meiotic cell cycle, with ncd^HL.ncd.Venus

(Hallen et al., 2008)

abnormal meiotic cell cycle, with ncd^TL.ncd.Venus

(Hallen et al., 2008)

abnormal meiotic cell cycle | female (with ncd^D)

(Apionishev et al., 2001)

abnormal meiotic cell cycle | oogenesis

(Hallen et al., 2008)

abnormal meiotic cell cycle | recessive

(Endow and Komma, 1997, Endow et al., 1990, Yamamoto et al., 1989)

abnormal mitotic cell cycle

(Endow and Komma, 1996, Hatsumi and Endow, 1992, Sequeira et al., 1989)

abnormal mitotic cell cycle, with ncd^HL.ncd.Venus

(Hallen et al., 2008)

abnormal mitotic cell cycle, with ncd^TL.ncd.Venus

(Hallen et al., 2008)

abnormal mitotic cell cycle | embryonic stage

(Hallen et al., 2008)

abnormal mitotic cell cycle | larval stage

(Cesario et al., 2006)

abnormal mitotic cell cycle | recessive

(Sharp et al., 2000, Endow and Komma, 1997, Endow et al., 1990)

lethal | recessive

(Endow and Komma, 1997)

lethal - all die during embryonic stage

(Hallen et al., 2008)

lethal - all die during embryonic stage | recessive

(Endow and Komma, 1998, Endow and Komma, 1996)

some die during embryonic stage

(Hallen et al., 2008)

some die during embryonic stage | recessive

(Endow and Komma, 1998, Endow and Komma, 1996)

Phenotype Manifest In

brain | larval stage

(Cesario et al., 2006)

meiosis & nuclear chromosome

(Endow et al., 1990)

meiosis & nuclear chromosome & oocyte

(Hatsumi and Endow, 1992)

meiosis & nuclear chromosome | female (with ncd^D)

(Apionishev et al., 2001)

meiosis II & spindle & egg

(Endow and Komma, 1998)

mitosis & nuclear chromosome

(Endow et al., 1990)

mitotic anaphase & spindle

(Hatsumi and Endow, 1992)

mitotic cell cycle

(Sharp et al., 2000)

mitotic metaphase & spindle

(Hatsumi and Endow, 1992)

spindle

(Sharp et al., 2000, Matthies et al., 1996)

spindle & oocyte

(Jang et al., 2005, Hatsumi and Endow, 1992)

Detailed Description

Statement

Reference

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.

(Hallen et al., 2008)

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.

(Cesario et al., 2006)

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.

(Cytrynbaum et al., 2005)

ncd¹ females have disorganised meiotic spindles in the oocyte.

(Jang et al., 2005)

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

(Wilson et al., 2004)

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.

(Brust-Mascher and Scholey, 2002)

ncd¹/ncd^D females show 32% X chromosome nondisjunction and 48% 4th chromosome nondisjunction.

(Apionishev et al., 2001)

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.

(Sharp et al., 2000)

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

(Sekelsky et al., 1999)

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.

(Sharp et al., 1999)

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.

(Endow and Komma, 1998)

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.

(Cook et al., 1997)

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

(Endow and Komma, 1997)

Mutants exhibit mitotic chromosome mis-segregation.

(Endow and Komma, 1996)

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.

(Matthies et al., 1996)

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 ncd^MC2/ncd^MC2 females have curved or bent spindles and split centrosomes at one or both spindle poles.

(Endow et al., 1994)

Axs^r2/+ ncd¹/+ females show much higher levels of both X and fourth chromosomal non-disjunction than do either of the single heterozygotes.

(Whyte et al., 1993)

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.

(Hatsumi and Endow, 1992)

Affects meiotic segregation of all chromosomes in females.

(Komma et al., 1991)

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

(Endow et al., 1990)

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.

(Sequeira et al., 1989)

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.

(Yamamoto et al., 1989)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

ncd¹ has lethal | embryonic stage | recessive phenotype, enhanceable by γTub37C¹²

(Endow and Komma, 1998)

ncd¹ has lethal | embryonic stage | recessive phenotype, enhanceable by γTub37C¹³

(Endow and Komma, 1998)

NOT Enhanced by

Statement

Reference

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

(Giunta et al., 2002)

Suppressed by

Statement

Reference

ncd^D/ncd¹ has abnormal meiotic cell cycle | female phenotype, suppressible by lwr⁰⁵⁴⁸⁶/lwr[+]

(Apionishev et al., 2001)

Enhancer of

Statement

Reference

ncd¹ is an enhancer of abnormal developmental rate phenotype of SAK^Ubi.GFP

(Basto et al., 2008)

ncd¹ is an enhancer of abnormal mitotic cell cycle phenotype of SAK^Ubi.GFP

(Basto et al., 2008)

ncd¹ is an enhancer of abnormal cytokinesis | larval stage phenotype of Klp61F⁰⁷⁰¹²

(Wilson et al., 2004)

NOT Enhancer of

Statement

Reference

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

(Giunta et al., 2002)

Suppressor of

Statement

Reference

ncd¹/ncd¹ is a suppressor of abnormal mitotic cell cycle phenotype of sub¹³¹/sub¹

(Cesario et al., 2006)

ncd¹ is a suppressor of lethal | larval stage phenotype of Klp61F^urc-1

(Wilson et al., 2004)

Other

Statement

Reference

ncd¹, sub¹³¹/sub¹ has lethal | third instar larval stage phenotype

(Cesario et al., 2006)

ncd[+]/ncd¹, sub¹³¹/sub¹ has viable | third instar larval stage phenotype

(Cesario et al., 2006)

Klp61F^urc-1/Klp61F⁰⁶³⁴⁵, ncd¹/ncd⁹ has partially lethal phenotype

(Wilson et al., 2004)

Klp61F⁰⁷⁰¹²/Klp61F⁰⁶³⁴⁵, ncd¹/ncd⁹ has viable phenotype

(Wilson et al., 2004)

Klp61F^urc-1, ncd¹ has increased occurrence of cell division phenotype

(Wilson et al., 2004)

Klp61F^urc-1/Df(3L)bab-PG, ncd¹ has lethal phenotype

(Wilson et al., 2004)

αTub67C³, ncd¹ has female sterile phenotype

(Komma and Endow, 1997)

Phenotype Manifest In

Suppressed by

Statement

Reference

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

(Apionishev et al., 2001)

Enhancer of

Statement

Reference

ncd¹ is an enhancer of phenotype of nod^a

(Knowles and Hawley, 1991)

ncd¹ is an enhancer of phenotype of nod⁴

(Knowles and Hawley, 1991)

ncd¹ is an enhancer of phenotype of nod³

(Knowles and Hawley, 1991)

ncd¹ is an enhancer of phenotype of nod²

(Knowles and Hawley, 1991)

ncd¹ is an enhancer of phenotype of nod⁶

(Knowles and Hawley, 1991)

NOT Enhancer of

Statement

Reference

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

(Giunta et al., 2002)

Suppressor of

Statement

Reference

ncd[+]/ncd¹ is a suppressor of organism | maternal effect | cleavage stage phenotype of αTub67C^kav-21g

(Gaspar and Szabad, 2009)

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

(Cesario et al., 2006)

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

(Wilson et al., 2004)

ncd¹ is a suppressor of aster & neuroblast & larva phenotype of Klp61F^urc-1

(Wilson et al., 2004)

ncd¹ is a suppressor of spindle & neuroblast & larva phenotype of Klp61F^urc-1

(Wilson et al., 2004)

Other

Statement

Reference

Klp61F⁰⁶³⁴⁵, ncd¹ has chromatin & spermatocyte phenotype

(Wilson et al., 2004)

Klp61F^urc-1, ncd¹ has nuclear lamina & neuroblast & larva phenotype

(Wilson et al., 2004)

Klp61F^urc-1/Klp61F⁰⁷⁰¹², ncd¹ has nuclear lamina & neuroblast & larva phenotype

(Wilson et al., 2004)

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

(Wilson et al., 2004)

Additional Comments

Genetic Interactions

Statement

Reference

The early cleavage defects seen in embryos derived from αTub67C^kav-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).

(Gaspar and Szabad, 2009)

ncd¹ enhances the developmental rate defects seen in flies expressing SAK^{Ubi.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 SAK^{Ubi.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 SAK^{Ubi.T:Avic\GFP} alone.

(Basto et al., 2008)

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

(Cullen et al., 2005)

Klp61F⁰⁶³⁴⁵ ncd⁹/Klp61F^urc-1 ncd¹ adults are recovered at 28% of the frequency expected for full viability. Biastral spindles are not found in Klp61F^urc-1 mutants, but comprise more than 66% of spindles in Klp61F^urc-1 ncd¹ mutants. More than 96% of Klp61F⁰⁷⁰¹² ncd¹ double mutant spindles are biastral. Klp61F^urc-1 ncd¹ double mutants survive longer as third instar larvae and show increased cell proliferation in comparison to Klp61F^urc-1 mutants. The nuclear lamina in interphase cells of Klp61F^urc-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/Klp61F^urc-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/Klp61F^urc-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.

(Wilson et al., 2004)

sub¹⁷⁹⁴ show allele specific interactions with alleles of ncd. sub¹⁷⁹⁴/+, ncd^D/+ 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.

(Giunta et al., 2002)

ncd¹/ncd^D female X and 4th chromosome nondisjunction is dominantly suppressed by lwr⁰⁵⁴⁸⁶.

(Apionishev et al., 2001)

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.

(Endow and Komma, 1998)

ncd¹/ncd¹ αTub67C³ females are sterile.

(Komma and Endow, 1997)

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

(Knowles and Hawley, 1991)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

ncd^P39

(Sekelsky et al., 1999)

ncd⁸

(Yamamoto et al., 1989)

ncd⁷

(Yamamoto et al., 1989)

ncd⁶

(Yamamoto et al., 1989)

ncd⁵

(Yamamoto et al., 1989)

Rescued by

ncd¹ is rescued by ncd^GFP(S65T)

(Hallen et al., 2008)

ncd¹ is rescued by ncd^FL.ncd.Venus

(Hallen et al., 2008)

ncd¹ is rescued by ncd^{nk11.GFP(S65T)}

(Sciambi et al., 2005)

ncd¹ is rescued by ncd^GFP

(Endow and Komma, 1996)

ncd¹ is rescued by ncd^GFP(S65T)

(Endow and Komma, 1996)

ncd¹ is rescued by ncd^+mEa

(Endow et al., 1994)

ncd⁷/ncd¹ is rescued by ncd^+t5.3

(Endow et al., 1990)

ncd¹ is rescued by ncd^+t11.5

(Yamamoto et al., 1989)

Partially rescued by

ncd¹ is partially rescued by ncd^GFP

(Endow and Komma, 1997)

ncd¹ is partially rescued by ncd^2.GFP(S65T)

(Endow and Komma, 1997)

ncd¹ is partially rescued by ncd^GFP(S65T)

(Endow and Komma, 1997)

ncd¹ is partially rescued by ncd^MC2

(Endow et al., 1994)

Not rescued by

ncd¹ is not rescued by ncd^HL.ncd.Venus

(Hallen et al., 2008)

ncd¹ is not rescued by ncd^TL.ncd.Venus

(Hallen et al., 2008)

ncd¹ is not rescued by ncd^2.GFP(S65T)

(Endow and Komma, 1996)

ncd¹ is not rescued by ncd^R6.9

(Yamamoto et al., 1989)

Comments

The chromosome segregation phenotype is almost completely rescued by ncd^T:Avic\GFP, and the embryo viability phenotype is partially rescued by two copies of ncd^T:Avic\GFP. Both phenotypes appear to completely rescued by four copies of ncd^T:Avic\GFP. Two copies of ncd^{T:Avic\GFP-S65T} partially rescue the ncd¹ phenotype, while four copies of ncd^{T:Avic\GFP-S65T} essentially completely rescue the ncd¹ phenotype.

(Endow and Komma, 1997)

Chromosome segregation and embryo viability can be rescued by 4 copies of ncd^{T:Avic\GFP-S65T}, 2 copies gives only partial rescue. Chromosome segregation and embryo viability can also be rescued by 4 copies of ncd^T:Avic\GFP, 2 copies gives only partial rescue. ncd^{2.T:Avic\GFP-S65T} fails to rescue both aspects of the phenotype.

(Endow and Komma, 1996)

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 ncd^MC2. Viability is also improved by ncd^MC2. 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 ncd^MC2. ncd^+mEa fully rescues the ncd¹ phenotype.

(Endow et al., 1994)

Images (0)

Mutant

Wild-type

Stocks (6)

Bloomington

1290

Df(3R)ca^nd1, e^s ncd¹ ca^nd1/In(3R)C, e¹ Dr^Mio ca¹

1720

Df(3R)ca^nd1, Sb¹ ss¹ Ubx^bx-34e e^s ncd¹ ca^nd1/TM3

60738

w¹¹¹⁸; P{ncd-gfp*}M3M1/SM5; Df(3R)ca^nd1, P{ncd-gfp*}M9F1 ncd¹ ca^nd1/TM3, Sb¹ Ser¹