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General Information
Symbol
Dmel\bowl1
Species
D. melanogaster
Name
FlyBase ID
FBal0051737
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C3780420A

Reported nucleotide change:

C1039A

Amino acid change:

S232term | bowl-PA; S232term | bowl-PB; S232term | bowl-PC; S232term | bowl-PD; S232term | bowl-PF; S232term | bowl-PG; S232term | bowl-PH

Reported amino acid change:

S232term

Comment:

5 residues upstream of first zinc finger

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

Amino acid replacement: S232term.

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

Homozygous clones generate cuticle patterning defects in the prescutum.

Homozygous clones induced in the third larval instar adopt a round and compact morphology and tend to segregate from the surrounding bowl[+] cells.

Somatic mutant clones induced in the antennal disc during L1 result in ectopic antennae formation, containing both proximal and distal antennal segments.

Mutant somatic clones in the ventral-posterior rim of the antennal disc lobe in L1 result in ventral eyelet formation and differentiation of mutant cells into photoreceptors in the adult eye.

Most homozygous clones generated at the early first larval instar in the disc proper of the wing disc survive.

Only 50% of homozygous clones generated at the early first larval instar in the peripodial epithelium of the wing disc survive, with most surviving near the disc stalk.

Homozygous clones generated at the second larval instar in the peripodial epithelium or disc proper of the wing disc both survive.

Homozygous clones in the eye disc (induced during the first larval instar) that span the margin cause either a delay in, or the inhibition of, retinal initiation.

Mutant clones in the distal parts of the leg are associated with tarsal segment fusions, as the joints fail to form within the mutant tissue. This joint loss is cell autonomous. In some cases where the mutant clone only forms a small part of the leg, no defects in segmentation are seen. In the proximal part of the leg, mutant clones are not associated with leg segment fusion, but rather with dark melanotic protrusions from the leg cuticle, which always occur near the site of an endogenous joint. Legs comprised almost entirely of mutant clone tissue (large clones induced using the Minute technique) show a failure of joint formation in segments extending from the tibia to tarsal segment 5, but proximal joints form normally.

Mutant embryos at stage 16 have hindguts about half the size of wild-type. These hindguts have larger lumens and two or three more cells in their circumference than those of wild-type. Hindguts are club shaped and smaller in both length and diameter. Hindgut epithelial cells are taller and narrower than seen in wild-type. The "boundary cells" that normally run the length of the large intestine are duplicated. Cell proliferation and apoptosis appear normal in mutant hindguts. Hindguts contain slightly fewer cells than wild-type. The visceral mesoderm is also normal in these mutants.

Homozygous embryos exhibit the 'tail-up' phenotype and defects in the mandible and maxilla. Hindgut is drastically reduced, proventriculus is absent. Second abdominal denticle belt is missing and the sixth abdominal denticle belt is defective in bowl1/bowl3 transheterozygotes. Lateralgraten is shortened and the ventral arm reduced in bowl1/bowl2 transheterozygotes.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT suppressed by
Statement
Reference

bowl1 has visible | somatic clone phenotype, non-suppressible by Antp73b

Phenotype Manifest In
NOT Enhanced by
Statement
Reference
NOT suppressed by
Statement
Reference
Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

Somatic mutant bowl1 clones induced in the ventral region of the antennal imaginal disc during stage L1 in Antp73b mutant larvae result in the formation of ectopic, supernumerary appendages.

Expression of drmScer\UAS.cGa under the control of Scer\GAL4Act5C.PP in clones in the eye disc in a bowl1 background does not result in ectopic retinogenesis.

drm3 bowl1 double mutant clones in the leg (induced using the Minute technique) have a leg segment fusion phenotype that can be attributed to the loss of bowl alone.

The gut morphology of Df(2L)drm-P2, bowl1homozygous embryos or drm3, bowl1 double homozygous embryos, is indistinguishable from that of either single mutant. linunspecified; bowl1 double homozygous embryos have a foregut phenotype identical to those of bowl1 homozygotes (narrow and lacking a keyhole structure), rather than linunspecified homozygotes (bloated and with an expanded keyhole structure). This phenotype is unaffected in embryos also homozygous for drm3, or Df(2L)drm-P2.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (3)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (13)