FlyBase Allele Report: Dmel\nod[a]

General Information

Symbol

Dmel\nod^a

Species

D. melanogaster

Name

FlyBase ID

FBal0013064

Feature type

allele

Associated gene

Dmel\nod

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

loss of function allele

amorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Rasooly et al., 1994)

hypomorphic allele - genetic evidence

(Murphy and Karpen, 1995)

loss of function allele

(Theurkauf and Hawley, 1992, Zhang and Hawley, 1990)

Mutagen

ethyl methanesulfonate

(Rasooly et al., 1994, Theurkauf and Hawley, 1992, Rasooly et al., 1991)

Progenitor genotype

Cytology

Description

Five nucleotide changes and a G to A transition, nonsense mutation at base pair 3765. Resulting protein is 12 amino acids shorter than wild type.

(Rasooly et al., 1994)

Putative point mutation.

(Knowles and Hawley, 1991)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

X:11,585,417..11,585,417 [+]

Nucleotide change:

G11585417A

Reported nucleotide change:

G3765A

Amino acid change:

W655term | nod-PA; W655term | nod-PB

Reported amino acid change:

??term

Comment:

G to A nucleotide change at the second or third position of the wild type Trp codon leads to a nonsense mutation (exact site of mutation unspecified). The mutation was annotated at the second base of the codon.

(Rasooly et al., 1994)

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 | female (with nod²)

(Apionishev et al., 2001)

Phenotype Manifest In

meiosis & nuclear chromosome | female (with nod²)

(Apionishev et al., 2001)

Detailed Description

Statement

Reference

nod^a/FM7a nod² females show 43% X chromosome nondisjunction and 89% 4th chromosome nondisjunction.

(Apionishev et al., 2001)

nod^a does not reduce the transmission of the Dp(1;f)1187 derivative P{PZ}8-23, but nod^a/nod³ reduces P{PZ}8-23 transmission to 9%.

(Murphy and Karpen, 1995)

Spindle organisation in nod^a/nod⁴ oocytes is generally normal, although asymmetrical spindles or normal spindles with spurs associated with one pole are occasionally seen. The X chromosomes rarely exchange in these oocytes. Spindle orientation of nonexchange chromosomes in nod^a/nod⁴ oocytes is highly variable and always abnormal, and the nonexchange chromosomes may be found free in the cytoplasm, or with both homologs present on the same half spindle. The free nonexchange chromosomes are often associated with spindle-like microtubule bundles. Single nonexchange chromosomes that are associated with a half-spindle are always positioned at the pole, not at the wild-type position between the plate and the pole. When more than one nonexchange chromosome is associated with a single half-spindle, one chromosome is always at the pole, but the other is positioned away from the pole, towards the metaphase plate. Homozygous nod^a females have similar oocyte defects as nod^a/nod⁴ females, except that the X chromosomes recombine at normal frequencies in homozygous nod^a oocytes, and free X chromosomes are seen at a much lower frequency.

(Theurkauf and Hawley, 1992)

The frequency of X chromosome non-disjunctions in nod^a mutants is increased by mei-S282¹, mei-218¹ or mei-9^b.

(Feany and Hawley, 1991)

Impairs distributive disjunction and induces nonexchange chromosome to undergo nondisjunction, as well as both meiotic and mitotic chromosome loss.

(Zhang and Hawley, 1990)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

nod²/nod^a has abnormal meiotic cell cycle | female phenotype, suppressible by lwr⁰⁵⁴⁸⁶/lwr[+]

(Apionishev et al., 2001)

Other

Statement

Reference

In(1)FM7, nod⁴/nod^a has abnormal meiotic cell cycle phenotype

(Cui and Hawley, 2005)

Phenotype Manifest In

Enhanced by

Statement

Reference

nod^a has phenotype, enhanceable by ncd¹

(Knowles and Hawley, 1991)

Suppressed by

Statement

Reference

nod²/nod^a has meiosis & nuclear chromosome | female phenotype, suppressible by lwr⁰⁵⁴⁸⁶/lwr[+]

(Apionishev et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

mei-38¹ nod^a double mutant females show an additive phenotype for chromosome nondisjunction; the frequency of X chromosome nondisjunction (8.9%) is similar to that of mei-38¹ single mutants and the frequency of 4th chromosome nondisjunction (71.4%) is similar to that of nod^a single mutants.

(Wu et al., 2008)

In(1)FM7 nod⁴/nod^a females show high levels of X and 4th chromosome nondisjunction (53.2% and 78.9% respectively) compared to control In(1)FM7 nod⁺ females. The majority of apparent 4th chromosome nondisjunction events result from loss of the 4th chromosome.

(Cui and Hawley, 2005)

nod^a/FM7a nod² female nondisjunction is dominantly suppressed by lwr⁰⁵⁴⁸⁶.

(Apionishev et al., 2001)

ncd¹ nod^a heterozygous females show an increased level of X and fourth chromosome nondisjunction.

(Knowles and Hawley, 1991)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially rescued by

nod⁴/nod^a is partially rescued by nod^UASp.EGFP/Scer\GAL4^{VP16.nanos.UTR}

(Cui and Hawley, 2005)