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General Information
Symbol
Dmel\tud1
Species
D. melanogaster
Name
FlyBase ID
FBal0017244
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
tudwc8, tudWC, tud1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

A21187422T

Amino acid change:

K1036term | tud-PA; K1033term | tud-PB

Reported amino acid change:

K1036term

Comment:

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

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: K1036term.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Female offspring of tud1/tudB45 mothers exhibit a significant reduction in the number of cap cells and terminal filament cells in the ovaries, as compared with wild type. The morphology and spatial arrangement of cap cells is similar to that in wild type.

Males born to mutant females are sterile but show normal copulation durations.

The progeny of homozygous tud1 mothers do not form a germline, while progeny of heterozyous tud1 mothers have a fully functional germline. There is little difference in lipid profiles between tud1 homozygous and heterozygous flies.

Expression of tudJOZ.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 fails to restore pole cell formation in eggs laid by tud1 mothers.

Expression of tud9A1.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 fails to restore pole cell formation in eggs laid by tud1 mothers.

Expression of tud3ZS.L-N.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 fails to restore pole cell formation in eggs laid by tud1 mothers.

Expression of tud3ZS.L-C.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 fails to restore pole cell formation in eggs laid by tud1 mothers.

Stage 4 tud1/Df(2R)PurP133a embryos show defective germ cell formation.

Expression of tudD7.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD8.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD9.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD10.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD11.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Embryos derived from tud1/Df(2R)PurP133a females have abdominal defects; only 9.1% have 8 wild-type abdominal segments, 43.8% have 0-2 abdominal segments, 29.5% have 3-5 abdominal segments and 31.0% have 6-8 abdominal segments (but with one segment reduced in size if 8 segments are present).

Nuage clusters and particles appear normal in mutant nurse cells.

Some polar granules appear normal in embryos derived from tud1/Df(2R)PF1 females, while others are greatly reduced.

A decreased number of polar granules compared to wild-type (about 1/6) are seen in homozygous mutant embryos. These granules are closely associated with mitochondria at the early cleavage stage. The number of mitochondria observed in the polar regions is also decreased by almost half.

Males derived from tud1 females lack sperm. Egg deposition is stimulated in wild-type females mated to these spermless males, but it begins later than in wild-type females mated to wild-type males and is at a consistently lower level. During the first day of mating, wild-type females mated to spermless males show a continuous decrease in the number of stage 13-14 oocytes and a rapid decrease followed by an increase in the number of oocytes at stages 10A-12, as occurs in wild-type females mated to wild-type males, although the decrease in stage 13-14 oocytes seen in wild-type females mated to spermless males is only 45% of that seen in wild-type females mated to wild-type males.

Males derived from tud1 females show little evidence of ability to displace first-mate sperm.

Females mated with sons of tud1 mothers only show a partial stimulation of oviposition during the first day after mating and lay about 60% of the clutch induced by mating with wild-type males. Oviposition declines to 30% of the full response during the second day and virtually reach virgin levels after 3 days. These females display nearly complete rejection of further mating 12 hours after copulation. Receptivity is recovered in about 50% of females after 1 day and in almost all females after two days. This differs from wild-type where subsequent matings are rejected for three days post copulation. When wild-type virgin females are mated with prdwt; prd4/Df(2L)Prl males (who are normally sterile, lacking accessory glands) followed by tud1 males (which are also normally sterile, lacking sperm) a few offspring are produced. However when this experiment is performed in reverse (copulation with tud1 males first) no restoration of fertility is seen.

The female progeny of homozygous females do not produce eggs. These eggless females store 19% fewer sperm than control females.

Male progeny of homozygous females do not produce sperm but produce normal quantities of accessory gland proteins. Females mated to these males are courted by males approximately half as vigorously as virgin females when tested 8 or 10 hours after the initial mating. When tested 24 hours after the initial mating, the attractiveness of the females is not significantly different from that of virgin females.

Normal seminal fluid, 'full' main-cell products, but no sperm. Female recipients of 'full' main-cell products (tud1) have significantly shorter lifespans than female recipients of 'reduced' (Cbβ\DT-AE148S.Acp95EF) or 'greatly reduced' main-cell products (Cbβ\DT-AE148D.Acp95EF), although they mated significantly less frequently.

Has no effect on the posterior accumulation of G-iα65A protein.

Males cannot transfer sperm to females when mating.

Males do not produce sperm. Females mated to tud1 males receive female accessory gland main cell secretions but no sperm display partial stimulation of oviposition on day 1 but little or no stimulation on subsequent days. Almost half of the females are receptive to control males one day after previously mating.

tud1;6xP{osk+108} embryos exhibit a tud phenotype.

Weak abdominal defects.

Absence of posterior pole plasm, polar granules and pole cells.

Does not interact with RpII140wimp maternal effect.

Progeny from tud1 mothers lack germ cells.

Embryos lack pole cells. Large amounts of vas protein are expressed in early stages of oogenesis. vas protein localizes to the posterior pole at the same stage of egg development as wild type, the protein disappears by early gastrulation.

Homozygous tud1 embryos and transheterozygous tud1/tud6 embryos derived from homozygous females have no polar granules, fail to form pole cells and have deletions of abdominal structures. vas and CycB transcripts are localized at the posterior.

The progeny of homozygous females have no pole cells.

Homozygous females produce embryos that fail to form pole cells, lack polar granules normally found at the posterior pole, and have deletions of abdominal segments.

Embryos derived from homozygous females show variable abdominal segment deletions. In some cases, the abdomen can be normal and the animals can survive to adulthood. The severity of the abdominal segment deletion phenotype is stronger in embryos derived from hemizygous females.

embryos from homozygous maternal-effect mutant mothers exhibit a so-called 'grandchildless-knirps' phenotype: all eggs lack polar granules and no pole cells are formed; most of the embryos show variable deletions of abdominal segments, whereby segment A4 is deleted most frequently; larger deletions may include segments A2 through A7; in extreme cases anterior parts of segment A1 become fused to posterior part of segment A8, but telson elements are always present and relatively normal. Around 30% of all embryos survive and grow into sterile adults. Analysis of germ-line clones indicates that the mutation is germ-line autonomous (Schupbach and Wieschaus, 1986a).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference

tud1 has abdomen phenotype, suppressible by nosN5

Additional Comments
Genetic Interactions
Statement
Reference

Injection of nosN5 RNA into hemizygous embryos completely rescues the abdominal phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of tudJOZ.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 fails to restore pole cell formation in eggs laid by tud1 mothers.

Expression of tud9A1.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 fails to restore pole cell formation in eggs laid by tud1 mothers.

Expression of tud3ZS.L.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 restores pole cell formation in eggs laid by tud1 mothers.

Expression of tud3ZS.L-N.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 fails to restore pole cell formation in eggs laid by tud1 mothers.

Expression of tud3ZS.L-C.vas.T:Avic\GFP-EGFP,T:Ivir\HA1 fails to restore pole cell formation in eggs laid by tud1 mothers.

Expression of tud7-11.nos.T:Ivir\HA1 rescues the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD7.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD8.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD9.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD10.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Expression of tudD11.nos.T:Ivir\HA1 fails to rescue the germ cell formation defects in tud1/Df(2R)PurP133a embryos.

Images (0)
Mutant
Wild-type
Stocks (6)
Notes on Origin
Discoverer

Wieschaus and Nusslein-Volhard.

Comments
Comments

Germline mosaic analysis shows that tud is required in the germline.

Although tud protein is present in mutant embryo extracts, its localization in the embryo is altered.

Microcauterised males are used as the controls for any difference in non-mating exposure to female survival.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (95)