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General Information
Symbol
Dmel\upd1YM55
Species
D. melanogaster
Name
FlyBase ID
FBal0013297
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
updYM55, upd4
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C18307422T

Reported nucleotide change:

C?T

Amino acid change:

Q60term | upd1-PA; Q60term | upd1-PB; Q60term | upd1-PC

Reported amino acid change:

Q60term

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

Amino acid replacement: Q55term.

Nucleotide substitution: C?T.

Amino acid replacement: ?60term.

Amino acid replacement: ??term.

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

upd1YM55/Df(1)os1 mutant flies have outstretched wings. Eye size is similar to wild type.

upd1YM55/Df(1)oso mutant flies have outstretched wings. Eye size is similar to wild type.

25% of upd1YM55 homozygous mutant embryos show defects in germ-band extension. Germ-band epithelial cells are normal in the head and dorsal-most regions of the embryo, however intercalating (ventrolateral) cells show a smaller apical cell surface. Germ-band cell intercalation is disrupted or, in extreme cases, blocked.

upd1YM55 embryos show a segmentation defect in which the A4 and A5 segments are fused.

The enlarged eye phenotype seen in flies carrying one copy of upd1GMR.PB is not modified if the flies are also carrying upd1YM55.

The pole cells of upd1YM55 mutant embryos are able to migrate normally and coalesce to form a pair of gonads in late embryos. However, one gonad often becomes located one segment offset from its proper location.

Migration of prospective border follicle cells in upd1sisC-5/upd1YM55 animals is delayed or defective. Marker analysis suggests that these cells are at least partially transformed to a nurse follicle cell fate.

Mosaic stage 9-10A follicles that have upd1[-] anterior polar cells contain fewer than normal border cells and the border cells fail to migrate. Morphologically normal stretched and centripetal cells are present in these follicles.

Mosaic stage 9-10 follicles that have upd1[-] posterior polar cells have a normally localised oocyte at the posterior part of the follicle and the oocyte nucleus is correctly positioned.

When homozygous somatic clones are made in the egg chamber, defects in border cell migration are seen. Whenever the polar cells are mutant, a complete failure in border cell migration is seen. However, in egg chambers in which the germ-line is mutant, no migration defect is seen. In mutant egg chambers the outer border cell clusters consist of an average of 2.2 cells, as compared to 6 in wild-type.

Homozygous clones within the eye field show no phenotype either in imaginal discs or in the adult eye. Clones adjacent to the optic stalk produce almost complete dorsalisation of the eye field as assayed by ommatidial polarity.

Defect in the fourth and fifth abdominal denticle belt. This does not produce embryonic lethality as mutant larvae, pupae and sometimes adult can develop lacking the abdominal region. T2, T3 and A8 are sometimes deleted, the head is usually involuted but most head structures are present. Germline clone analysis of os alleles of the upd complementation group indicate they are not required for germline viabilty and do not have a maternal effect. Zygotic lethality acts in the embryo, larval and pupal stages.

Interacts with RpII140wimp maternal effect.

embryonic lethal. Mutants show variable larval cuticular phenotype with defects predominantly in the mesothorax and the fifth abdominal segment (Nusslein-Volhard et al., 1984; Gergen and Wieschaus, 1986); also some head defects and fourth, sixth, seventh and eighth abdominal segment defects. Heterozygotes show 88-93% viability (Wieschaus and Noell, 1986). T2 defect; rudimentary filzkorper and posterior spiracles; A6 and A7 denticle belts fused; A8 denticle belt reduced

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

upd1YM55 is an enhancer of lethal phenotype of hop25/hop29

upd1YM55 is an enhancer of lethal phenotype of hopM637/hop25

upd1YM55 is an enhancer of partially lethal phenotype of hop3/hop25

NOT Suppressor of
Statement
Reference

os[+]/upd1YM55 is a non-suppressor of neuroanatomy defective phenotype of spin10403

Other
Phenotype Manifest In
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference

upd1YM55 has phenotype, non-suppressible by eRF1[+]/eRF1F2

Enhancer of
Statement
Reference

os[+]/upd1YM55 is an enhancer of egg chamber phenotype of hop27/hop25

NOT Suppressor of
Statement
Reference

os[+]/upd1YM55 is a non-suppressor of eye disc phenotype of spin10403

os[+]/upd1YM55 is a non-suppressor of glial cell phenotype of spin10403

Additional Comments
Genetic Interactions
Statement
Reference

The glial overmigration phenotype seen in spin10403 eye discs is not suppressed if the animals are also heterozygous for upd1YM55.

An average of 4.5% upd1YM55, sqhAX3 homozygous mutant embryos show germ-band extension defects, much reduced compared to upd1YM55 homozygous mutant embryos. Ectopic apical cell constriction defects are rescued in upd1YM55, sqhAX3 homozygous mutant embryos.

An average of 6% upd1YM55, Rho1k02107b homozygous mutant embryos show germ-band extension defects, much reduced compared to upd1YM55 homozygous mutant embryos.

The reduced ectodermal apical cell surface size observed in upd1YM55 mutant embryos at mid germ-band extension is rescued in upd1YM55; WASp3/+ embryos.

The pupal lethality of Df(2R)P3C homozygotes is partially suppressed by upd1YM55/+.

92% of hop25 upd1YM55/hop27 egg chambers are fused and the number of extra polar cells is increased compared to hop25/hop27 single mutants.

Dominantly enhances the phenotype of hop25 in transheterozygous combination with hop27, hop14, hop3, hop12, hop33, hop32, hopM637 or hop29.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of upd1Scer\UAS.cZa under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 rescues the germ-band extension and apical cell shape defects observed in upd1YM55 mutant embryos.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Maternal germline clonal analysis demonstrates there is no maternal effect.

External Crossreferences and Linkouts ( 1 )
Crossreferences
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
Synonyms and Secondary IDs (8)
References (26)