Gene Dmel\nod

Experimentally Determined Recombination Data

Location

1-36

1-35.5

Left of (cM)

Right of (cM)

Notes

Based on mapping of nod^DTW.

Molecular Map Data

Gene Order (in direction of increasing cytology)

References

Gene Order (overall orientation not stated)

References

Overall orientation not stated: roX2+ nod+

(Amrein and Axel, 1997)

Gene Model & Products

Please see the GBrowse view of Dmel\nod for information on other features

Comments on Gene Model

Transcript Data

Annotated Transcripts

Name

FlyBase ID

RefSeq ID

Length (nt)

Associated CDS (aa)

nod-RA

FBtr0073516

NM_078570

2407

666

Additional Transcript Data & Comments

Reported size (kB)

2.4 (northern blot)

Comments

External Data

Crossreferences

Polypeptide Data

Annotated Polypeptides

Name

FlyBase ID

Predicted MW (kD)

Length (aa)

Theoretical pI

RefSeq ID

GenBank protein

nod-PA

FBpp0073363

73.9

666

10.19

NP_511125

AAF48064

Additional Polypeptide Data & Comments

Reported size (kD)

666 (aa); 74 (kD)

(BDGP Project Members, 2000-, Gilliland, 2003.1.7, Mukai et al., 2006)

Comments

External Data

Linkouts

PANTHER - Protein classification by function, families, and pathways

•

FBgn0002948

Crossreferences

InterPro domains - A database of protein families, domains, and functional sites

•

Helix-hairpin-helix motif (IPR000445)

Kinesin, motor region (IPR001752)

Helix-hairpin-helix DNA-binding, class 1 (IPR003583)

Sequences Consistent with the Gene Model

DDBJ /
EMBL /
GenBank

DNA sequence

Protein sequence

Name

P18105

UniProtKB/TrEMBL

Maps to

Does NOT map to

Identified with

SD02282

D1032

(BDGP Project Members, 1994-1999)

Mapped Features & Mutations

Please see GBrowse or insertion reports for information on insertions of transgenic constructs and features not listed here

Type

Symbol & Location

Additional Notes

References

deletion

nod[4]
X:11,474,958..11,475,142

evidence=experimental
comment=Mutation consists of an 8bp deletion located in this region resulting in a frameshift and a stop codon after 40 amino acids.

(Rasooly et al., 1994, Afshar et al., 1995)

point mutation

nod[DTW]
X:11,475,301..11,475,301

reported_pr_change=S94N
evidence=experimental
pr_change=S94N|nod-PA
reported_na_change=G352A
na_change=G11475301A

point mutation

nod[DR2]
X:11,475,541..11,475,541

comment=Position of mutation on reference sequence inferred by FlyBase curator.
evidence=experimental
pr_change=D151N|nod-PA
reported_na_change=G523A
reported_pr_change=D151R
na_change=G11475541A

point mutation

nod[DR3]
X:11,475,671..11,475,671

evidence=experimental
pr_change=R194H|nod-PA
reported_na_change=G649A
reported_pr_change=R194H
na_change=G11475671A

point mutation

nod[a]
X:11,479,450..11,479,451

reported_pr_change=??@
pr_change=W655@|nod-PA
reported_na_change=G3765A
comment=G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation (exact site of mutation unspecified) Other mutations might be present in this strain.
evidence=experimental

(Rasooly et al., 1994)

External Data

Linkouts

DEDB - Drosophila exon database: splicing graphs

•

2517

Crossreferences

Expression Data

FlyBase-Curated Data

Transcript and
Protein data

Please see the FlyBase Gene Expression Report for details of gene expression from the literature.

Summary of Transcript Expression

Stage

Tissue/Position

Reference

oogenesis stage,adult stage

germarium

oogenesis stage,adult stage | stage S1-S3

ovariole

embryonic stage-adult stage

meiotic cell cycle defective

Marker for

Subcellular Localization

CV Term

Summary of Polypeptide Expression

Stage

Tissue/Position

Reference

Marker for

Subcellular Localization

CV Term

Microarray Data

Developmental timecourse, Costello et al., 2008 (Original data from Arbeitman et al., 2002)

Untitled Document detailed view

AI531306

External Data & Images

Linkouts

FLIGHT - Cell culture data for RNAi and other high-throughput technologies

•

FBgn0002948

FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array

•

FBgn0002948

GEO (NCBI) - Gene expression data: microarray and other high-throughput technologies

•

FBgn0002948

Alleles & Phenotypes

Summary of Allele Phenotypes

Lethality

Allele

viable

lethal | recessive | conditional - cold sensitive

nod^DTW

lethal | male | conditional - cold sensitive

nod^DR4

Other Phenotypes

Allele

nod⁴

meiotic cell cycle defective | recessive

meiotic cell cycle defective | dominant

meiotic cell cycle defective | dominant | female

nod^DTW

meiotic cell cycle defective | female (with nod^a)

nod²

meiotic cell cycle defective | female (with nod²)

nod^a

meiotic cell cycle defective | female | conditional - cold sensitive

nod^DTW

mitotic cell cycle defective

nod^DTW

Sterility

Allele

fertile

Phenotype manifest in

Allele

meiosis & nuclear chromosome | female (with nod^a)

nod²

meiosis & nuclear chromosome & oocyte

nod⁴

meiosis & nuclear chromosome | female

nod^DTW

meiosis & nuclear chromosome | female (with nod²)

nod^a

mitosis & nuclear chromosome

nod^dsRNA.cGa

polytene chromosome chromocenter

nod^unspecified

Classical Alleles ( 19 )

For All Classical Alleles Show

Allele of nod	Class	Mutagen	Stocks	Known lesion
nod¹		γ ray	0	Yes
nod²		γ ray spontaneous	2	Yes
nod³	loss of function	γ ray	2	Yes
nod⁴	amorph, loss of function	γ ray	2	Yes
nod⁵	loss of function	γ ray	0	--
nod⁶	loss of function	γ ray	0	Yes
nod⁹		natural population	0	Yes
nod^A4579T		natural population	0	--
nod^DR1	loss of function	ethyl methanesulfonate	0	Yes
nod^DR2	loss of function	ethyl methanesulfonate	0	--
nod^DR3	loss of function	ethyl methanesulfonate	1	--
nod^DR4		ethyl methanesulfonate	0	--
nod^DTW	antimorph	ethyl methanesulfonate	2	Yes
nod^EY01772		P-element activity	1	--
nod^a	amorph, loss of function, hypomorph	ethyl methanesulfonate	2	Yes
nod^e03334		piggyBac transposase	1	--
nod^f01431		piggyBac transposase	1	--
nod^f04008		piggyBac transposase	2	--
nod^unspecified			0	--

Alleles Carried on Transgenic Constructs ( 16 )

For All Alleles Carried on Transgenic Constructs Show

Allele of nod	Mutagen	Stocks	Known lesion
nod^{C.hs.T:Zzzz\FLAG}	in vitro construct \| coding region fusion in vitro construct \| regulatory fusion	0	Yes
nod^{CN1.hs.T:Zzzz\FLAG}	in vitro construct \| coding region fusion in vitro construct \| regulatory fusion	0	Yes
nod^{CN2.hs.T:Zzzz\FLAG}	in vitro construct \| coding region fusion in vitro construct \| regulatory fusion	0	Yes
nod^{CN3.hs.T:Zzzz\FLAG}	in vitro construct \| coding region fusion in vitro construct \| regulatory fusion	0	Yes
nod^{CN4.hs.T:Zzzz\FLAG}	in vitro construct \| coding region fusion in vitro construct \| regulatory fusion	0	Yes
nod^GD16725	in vitro construct \| RNAi in vitro construct \| regulatory fusion	2	Yes
nod^GD8802	in vitro construct \| RNAi in vitro construct \| regulatory fusion	0	Yes
nod^{N.hs.T:Zzzz\FLAG}	in vitro construct \| coding region fusion in vitro construct \| regulatory fusion	0	Yes
nod^{NDD1-2.Scer\UAS.P\T.T:Avic\GFP-EGFP}	in vitro construct \| regulatory fusion in vitro construct \| coding region fusion in vitro construct \| amino acid replacement in vitro construct \| site directed mutagenesis	0	Yes
nod^{NDD3.Scer\UAS.P\T.T:Avic\GFP-EGFP}	in vitro construct \| regulatory fusion in vitro construct \| coding region fusion in vitro construct \| amino acid replacement in vitro construct \| site directed mutagenesis	0	Yes
nod^{NDD4.Scer\UAS.P\T.T:Avic\GFP-EGFP}	in vitro construct \| regulatory fusion in vitro construct \| coding region fusion in vitro construct \| amino acid replacement in vitro construct \| site directed mutagenesis	0	Yes
nod^{Scer\UAS.P\T.T:Avic\GFP-EGFP}	in vitro construct \| regulatory fusion in vitro construct \| coding region fusion	0	Yes
nod^{Scer\UAS.P\T.T:Avic\GFP}	in vitro construct \| regulatory fusion in vitro construct \| coding region fusion	0	Yes
nod^dsRNA.cGa	in vitro construct \| RNAi	0	Yes
nod^{hs.T:Zzzz\FLAG}	in vitro construct \| coding region fusion in vitro construct \| regulatory fusion	0	Yes
nod^t4.0	in vitro construct \| genomic fragment	0	Yes

Aneuploid Aberrations

Useful deficiency

Df(1)m259-4

Disrupted in

Df(1)52

(Meller and Rattner, 2002)

Df(1)HA85

(Voelker et al., 1985, Cook et al., 1997)

Df(1)N71

(Voelker et al., 1985, Rasooly et al., 1991)

Df(1)m259-4

(Voelker et al., 1985, Zhang et al., 1990)

Df(1)v-N48

Df(1)v65b

(Voelker et al., 1985, Zhang et al., 1990)

Not disrupted in

Df(1)GA112

Df(1)HM456

Df(1)RA37

Not duplicated in

Dp(1;2)v⁺75d

Dp(1;Y)v⁺y⁺

Duplicated in

Dp(1;2)v⁺65b

Dp(1;3)v⁺74c

Dp(1;Y)y⁺v⁺#3

Transgenic Constructs & Insertions

Transgenic Constructs

Type of construct

Name

Expression data

UAS construct

P{GD16725}

P{GD8802}

P{UASp-nod-EGFP.NDD1-2}

P{UASp-nod-EGFP.NDD3}

P{UASp-nod-EGFP.NDD4}

P{UASp-nod-EGFP}

P{UASp-nod-GFP}

characterization construct

P{NZ}

P{UAS-Khc::nod::lacZ}

P{UAS-nod.GFP}

P{UASp-Khc::nod::lacZ}

heat-shock construct

Insertions

Type of insertions

Name

Expression data

miscellaneous insertions

insertion of mobile activating element

P{EPgy2}nod^EY01772

Related Comments

Please look at the allele reports for the complete phenotype data

Females homozygous for nod alleles exhibit high frequencies of meiotic chromosome loss and nondisjunction at meiosis I. Most nod-induced nondisjunctional events involve nonexchange chromosomes. For example, in nod/nod females nondisjunction frequencies for the always nonexchange fourth chromosomes approaches 90% (the vast majority of gametes are nullo-4 ova), whereas nonexchange X chromosomes apparently disjoin at random. Both the frequency of exchange and the disjunction of exchange bivalents was shown to be normal in nod/nod females. Thus, with respect to its role in meiosis, the nod⁺ function appears to be limited to the distributive segregation system. Based on an analysis of secondary nondisjunction in nod^a/nod^a females, Carpenter concluded that the nod defect does not impair the process of partner choice within the distributive system, but rather specifically impairs the disjunctional process. Nonexchange chromosomes derived from nod^a/nod^a mothers also undergo nondisjunction and presumably loss, at meiosis II. In addition, chromosomes derived from nod^a/nod^a mothers are mitotically unstable. nod-induced mitotic chromosome loss is restricted to maternal nonexchange chromosomes and does not exert any discernible effect on meiosis in males or on mitotic chromosome stability (Baker, Carpenter and Ripoll, 1978). Although none of the existing nod alleles is lethal or female sterile, the dosage-sensitive antimorphic mutation l(1)TW6 (Wright, 1973) is argued to be allelic to nod on the basis of three lines of evidence. First, l(1)TW6/+ females display a meiotic phenotype that is virtually identical to that exhibited by nod^a/nod^a females. Second, the two loci map to the same position on the X chromosome (Wright, 1973; Baker). Third, a γ-ray induced revertant of l(1)TW6 was shown to be a recessive nod allele (New and Hawley).

nod protein is a member of the kinesin superfamily so it is proposed that the nod locus encodes a spindle motor that is required to hold distributively paired chromosomes at the metaphase plate until anaphase.

(Murphy and Karpen, 1995)

nod gene product is required for nonexchange chromosomes.

(Zhang and Hawley, 1990)

Mutations at nod do not disrupt meiotic spindle formation and show no interaction with Axs.

(Whyte et al., 1993)

The sequence of the nod protein has been compared with the sequences of a variety of kinesin family proteins.

(Goodson et al., 1994)

nod is required for the correct segregation of the non-exchange chromosomes during meiosis, mutations result in a high level of nondisjunction of the non-exchange fourth chromosomes and achiasmate X chromosomes.

(Afshar et al., 1995)

The nonmotor domain of the nod protein can mediate direct binding to DNA. During prometaphase nod protein is localized on oocyte chromosomes and is not restricted to either specific chromosomal regions or to the kinetochore. Thus motor-based chromosome-microtubule interactions are not limited to the centromere but extend along the chromosome arms, providing a molecular explanation for the polar ejection force.

(Afshar et al., 1995)

Transmission of the Dp(1;f)1187 minichromosome is sensitive to the dosage of nod⁺. Multiple regions of Dp(1;f)1187 interact with nod⁺ to promote normal chromosome transmission. Most nod⁺ interactions are observed with regions that are not essential for centromere function.

An 82 amino acid residue segment of the tail of the nod protein is necessary for the localisation of the protein onto chromosomes.

(Afshar et al., 1995)

Examination of meiotic prophase in nod mutants reveals that while heterochromatic pairing may be a component of the mechanism of homologous segregation, it is not sufficient to guarantee proper disjunction of nonexchange homologs.

(Dernburg et al., 1996)

nod, a female-specific gene expressed in the ovary, is closely linked to roX2, a gene encoding an RNA with no apparent reading frame that shows male-specific expression in the adult fly.

(Amrein and Axel, 1997)

The reciprocal location of nod and Khc fusion proteins indicates microtubule polarity in the oocyte, epithelium, neuron and muscle.

(Clark et al., 1997)

nod is necessary for chromosome segregation and can interact specifically with the centromere. nod requires extracentromeric regions for its action in chromosome segregation.

(Cook et al., 1997)

RNAi screen using dsRNA made from templates generated with primers directed against this gene results in chromosome misalignment on the metaphase spindle when assayed in S2 cells. This phenotype can be observed when the screen is performed with or without Cdc27 dsRNA.

(Goshima et al., 2007)

Gene Ontology: Function, Process & Cellular Component ( 10 )

Molecular Function

CV term

Evidence

References

ATP binding

inferred from electronic annotation with InterPro:IPR001752

(FlyBase Curators et al., 2004-)

microtubule motor activity

inferred from mutant phenotype