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General Information

Symbol

Dmel\Neurl4^Δ1

Species

D. melanogaster

Name

FlyBase ID

FBal0316516

Feature type

allele

Associated gene

Dmel\Neurl4

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Jones and Macdonald, 2015)

Progenitor genotype

P{EPgy2}Neurl4^EY12221

(Jones and Macdonald, 2015)

Cytology

Description

Imprecise excision ofP{EPgy2}Neurl4^EY12221. A small portion of the P-element remains.

(Jones and Macdonald, 2015)

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

female semi-sterile |maternal effect

(Jones and Macdonald, 2015)

viable

(Jones and Macdonald, 2015)

Phenotype Manifest In

oocyte

(Jones and Macdonald, 2015)

primordial germ cell |embryonic stage 4 |maternal effect

(Jones and Macdonald, 2015)

primordial germ cell |embryonic stage 5 |maternal effect

(Jones and Macdonald, 2015)

primordial germ cell |embryonic stage 10 |maternal effect

(Jones and Macdonald, 2015)

Detailed Description

Statement

Reference

Neurl4^Δ1 mutants display a dominant misshapen primordial germ cells (PGC) in well over half of the embryos from heterozygous mothers. The frequency of PGC defects is similar in progeny embryos ofNeurl4^Δ1/+ females crossed with eitherNeurl4^Δ1 or wild-type males, demonstrating that the PGC phenotype is independent of zygotic genotype. Embryos from wild-type females crossed to homozygousNeurl4^Δ1 males do not shot the PGC phenotype.

Embryos fromNeurl4^Δ1 mutant mothers show multiple PGC defects at stage 10 during migration: the protrusion on PGCs are often smaller than normal; there are displaced vesicles just as seen in stage 5 embryos; and some PGCs are elongated relative to those in wild-type embryos.

Neither wild-type norNeurl4^Δ1/+ mutant stage 5 embryos PGCs are positive for a marker of apoptosis.

Homozygous or hemizygous mutants are viable and appear healthy. However, a fraction of the progeny ofNeurl4^Δ1 mutant mothers are agametic and thus infertile. Examination of embryos fromNeurl4^Δ1 mutant mothers reveals that, in addition to the abnormal PGC morphology, the number of PGCs is reduced compared with wild-type.

(Jones and Macdonald, 2015)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Suppressed by

Statement

Reference

Neurl4^Δ1 hasprimordial germ cell |maternal effect |embryonic stage 5 phenotype, suppressible byHmgcr^11.5/Hmgcr[+]

(Jones and Macdonald, 2015)