FlyBase Allele Report: Dmel\sub[1794]

General Information

Symbol

Dmel\sub¹⁷⁹⁴

Species

D. melanogaster

Name

FlyBase ID

FBal0135614

Feature type

allele

Associated gene

Dmel\sub

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Giunta et al., 2002)

Mutagen

ethyl methanesulfonate

(Giunta et al., 2002)

Progenitor genotype

Cytology

Description

Amino acid replacement: C152Y.

(Giunta et al., 2002)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:17,747,524..17,747,524 [-]

Nucleotide change:

G17747524A

Amino acid change:

C152Y | sub-PA; C152Y | sub-PB

Reported amino acid change:

C152Y

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Giunta et al., 2002)

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 (with Df(2R)Pcl^XM82)

(Giunta et al., 2002)

abnormal meiotic cell cycle (with sub¹)

(Giunta et al., 2002)

abnormal meiotic cell cycle (with sub^Dub)

(Giunta et al., 2002)

abnormal meiotic cell cycle | recessive

(Giunta et al., 2002)

abnormal mitotic cell cycle | maternal effect | recessive

(Giunta et al., 2002)

female semi-fertile (with sub^Dub)

(Giunta et al., 2002)

female semi-fertile | recessive

(Giunta et al., 2002)

female sterile (with sub¹), with Scer\GAL4^{VP16.nanos.UTR}, sub^CT.UASp.EGFP

(Jang et al., 2007)

Phenotype Manifest In

chromosome, centromeric region (with Df(2R)PC4)

(Giunta et al., 2002)

karyosome

(Giunta et al., 2002)

karyosome (with Df(2R)Pcl^XM82)

(Giunta et al., 2002)

karyosome (with sub^Dub)

(Giunta et al., 2002)

spindle

(Giunta et al., 2002)

spindle (with Df(2R)Pcl^XM82)

(Giunta et al., 2002)

spindle (with sub^Dub)

(Giunta et al., 2002)

Detailed Description

Statement

Reference

Expression of sub^{CT.Scer\UAS.P\T.T:Avic-EGFP} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} in sub¹⁷⁹⁴/+ females results in reduced numbers of progeny.

Expression of sub^{CT.Scer\UAS.P\T.T:Avic-EGFP} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} in sub¹⁷⁹⁴/sub¹ females results in sterility.

(Jang et al., 2007)

Elevated frequency of X, fourth and second chromosome non-disjunction. Autosomal chromosome loss is significant. Most or all of the non-disjunction involves homologs at meiosis I. The position of the chiasma seems to have little effect on whether the homologs will fail to segregate normally. Achiasmate chromosomes require sub for segregation, whereas chiasmate bivalents can in some instances segregate correctly. Transheterozygotes with sub¹ show elevated levels of X chromosome non-disjunction in females. Stage 14 oocytes of sub¹⁷⁹⁴ homozygotes and transheterozygotes with sub^Dub show a defect in spindle pole formation - most often spindles are either monopolar or tripolar, karyosome may be split, spindles broken or misshapen such that they fray, or do not taper at the poles. When heterozygous with Df(2R)Pcl^XM82 a higher frequency of spindle defects results, though the severity of spindle defects when they occur is unchanged. In stage 14 oocytes of sub¹⁷⁹⁴/Df(2R)PC4 females the centromeres are often abnormally arranged: either on the same side of the karyosome or, if the karyosome is split, in the same mass of chromosomes. Eggs derived from sub¹⁷⁹⁴ mothers show some abnormalities in spindle morphology during early mitoses, though later stage embryos develop normally suggesting recovery from the early defect mitotic defect.

(Giunta et al., 2002)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

sub¹⁷⁹⁴ has abnormal meiotic cell cycle phenotype, enhanceable by ncd^D/ncd[+]

(Giunta et al., 2002)

sub¹⁷⁹⁴ has abnormal meiotic cell cycle phenotype, enhanceable by nod[+]/nod⁴

(Giunta et al., 2002)

NOT Enhanced by

Statement

Reference

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

(Giunta et al., 2002)

Enhancer of

Statement

Reference

sub[+]/sub¹⁷⁹⁴ is an enhancer of abnormal meiotic cell cycle phenotype of ncd^D

(Giunta et al., 2002)

sub[+]/sub¹⁷⁹⁴ is an enhancer of abnormal meiotic cell cycle phenotype of nod⁴

(Giunta et al., 2002)

NOT Enhancer of

Statement

Reference

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

(Giunta et al., 2002)

Phenotype Manifest In

Enhanced by

Statement

Reference

sub¹⁷⁹⁴ has karyosome phenotype, enhanceable by ncd^D/ncd[+]

(Giunta et al., 2002)

sub¹⁷⁹⁴ has spindle phenotype, enhanceable by ncd^D/ncd[+]

(Giunta et al., 2002)

NOT Enhanced by

Statement

Reference

sub¹⁷⁹⁴ has spindle phenotype, non-enhanceable by ncd¹/ncd¹

(Giunta et al., 2002)

Enhancer of

Statement

Reference

sub[+]/sub¹⁷⁹⁴ is an enhancer of karyosome phenotype of ncd^D

(Giunta et al., 2002)

sub[+]/sub¹⁷⁹⁴ is an enhancer of spindle phenotype of ncd^D

(Giunta et al., 2002)

Additional Comments

Genetic Interactions

Statement

Reference

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. Df(2R)PC4/+, ncd^D/+ shows less nondisjunction than sub¹⁷⁹⁴/+, ncd^D/+. sub¹⁷⁹⁴ show a less strong, but still significant, interaction with nod⁴ than with ncd^D. Stage 14 oocytes of sub¹⁷⁹⁴/+, ncd^D/+ show a defect in spindle pole formation - most often spindles are either monopolar or tripolar, karyosome may be split, spindles broken or misshapen such that they fray, or do not taper at the poles. 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)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

sub¹

(Giunta et al., 2002)

sub^Dub

(Giunta et al., 2002)

Rescued by

sub^unspecified/sub¹⁷⁹⁴ is rescued by sub^UASp.EGFP/Scer\GAL4^{VP16.nanos.UTR}

(Jang et al., 2007)

Not rescued by

sub^unspecified/sub¹⁷⁹⁴ is not rescued by sub^CT.UASp.EGFP/Scer\GAL4^{VP16.nanos.UTR}

(Jang et al., 2007)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

Allelic series (strongest to weakest phenotype): sub¹³¹/sub^Dub = sub²⁰²/sub^Dub = sub²¹⁸/sub^Dub = sub²²/sub^Dub = sub⁷²/sub^Dub = sub¹⁰⁴/sub^Dub = sub¹⁵⁸/sub^Dub > sub¹⁷⁹⁴/sub^Dub > +/sub^Dub.

(Giunta et al., 2002)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

sub¹⁷⁹⁴

(Das et al., 2018, Jang et al., 2007, Jang et al., 2005)

Name Synonyms

Secondary FlyBase IDs

References (5)

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