Open Close
General Information
Symbol
Dmel\bib1
Species
D. melanogaster
Name
FlyBase ID
FBal0001125
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
bibID05, bibID105
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
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
Phenotype Manifest In
Detailed Description
Statement
Reference

When single cell mutant clones are made, duplications of class I neurons.

en and nub expressing multidendritic (md) neurons in the dorsal cluster are moderately over produced in bib1 mutants.

Homozygous mutant somatic clones in the eye contain occasional extra photoreceptor cells. Ommatidia often have extra photoreceptor cell rhabdomeres.

Homozygous clones in adult flies have moderately increased numbers of macrochaetae and microchaetae. These bristles have normal sockets innervated by single neurons.

Homozygous embryos have an increased number of cardiac precursor cells.

Embryos exhibit fused muscles in patterned arrangements, particularly in the more dorsal regions of the embryo. The birefringent is clearly correlated with the expansion of the CNS and PNS, and the loss of epidermis and the degree to which myoblast fusion occurs. Where myoblast fusion fails conspicuous clusters of mesodermal cells are formed and if epidermal territories are expanded cells in these clusters may be recruited to fusion.

Sensory neurons, foregut, trachea, endoderm, and larval midgut are wild type.

ac protein distribution in bib1 embryos show ac expression is not restricted to a single cell of an ectodermal cell cluster, instead most cells of the cluster retain ac expression at a high level, enlarge, delaminate and become neuroblasts.

bib1 expression was not modified by the presence of ASC loss-of-function mutations.

Homozygous clones induced in the eye and thoracic imaginal discs show epidermal development indistinguishable from wild-type.

Intermediate embryonic neurogenic phenotype. CNS hypertrophy and epidermal defects are evident in all mutants.

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

bib[+]/bib1 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, fruNP0021

NOT Suppressor of
Statement
Reference

bib1 is a non-suppressor of phenotype of sno71e3

Additional Comments
Genetic Interactions
Statement
Reference

A bib1 background enhances the rough eye phenotype related to fru isoform B, found upon expression of fruNP0021 under the control of Scer\GAL4GMR.PF.

No effect on the faf eye phenotype.

No significant effect on the scaMSKF mutant phenotype.

There is no detectable dominant interaction with sno71e3.

Does not rescue the lethality conferred by NAx-E2/NAx-9 heterozygotes.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Nusslein-Volhard and Wieschaus.

The Mon1mut4 allele is a background mutation present on some bib1 chromosomes, and it accounts for the aberrant protein trafficking phenotype that was erroneously attributed to bib1 in FBrf0204892.

Comments
Comments

Phenotype not modified by increasing the number of wild type alleles of amx, neur, N, Dl or E(spl).

Clonal analysis indicates that bib functions autonomously to inhibit neural development.

The bib1 mutant stock used in FBrf0204892 carries an unlinked mutation that accounts for some of the N-related findings originally attributed to bib in FBrf0204892. FBrf0204892 has thus been retracted. FlyBase curator comment: FBrf0221616 describes the characterisation of the unlinked mutation, showing that it is a mutation in Mon1.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (40)