When single cell mutant clones are made, duplications of class I neurons.
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.
Strong allele.
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.
bib1 is an enhancer of visible phenotype of Nsf2EQ.UAS, Scer\GAL4bbg-C96
bib[+]/bib1 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, fruNP0021
bib1 is an enhancer of wing margin phenotype of Nsf2EQ.UAS, Scer\GAL4bbg-C96
Nusslein-Volhard and Wieschaus.
Separable from: Mon1mut4.
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.
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 FBrf0204892 has thus been retracted.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.