Stop-codon suppression (UGA) postulated; FBrf0216884.
Gene model reviewed during 5.44
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.52
None of the polypeptides share 100% sequence identity.
Phosphorylated at its C-terminus.
Aquaporins contain two tandem repeats each containing three membrane-spanning domains and a pore-forming loop with the signature motif Asn-Pro-Ala (NPA).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\bib using the Feature Mapper tool.
Comment: reported as pericardial cell specific anlage
bib transcript is detected in all somatic cells at the start of cellularization. By the completion of cellularization, bib is absent from a 17-cell-wide ventral strip which includes the presumptive mesoderm cells and two rows of ectodermal cells. Through stage 8, bib expression is maintained in most ectodermal tissue. During neuroblast delamination at late stage 8-stage 9, neuroblasts which segregate from the ectodermal layer lose bib expression. At the end of germ-band extension, the mesoderm begins to express bib. By late stage 11, bib expression disappears first from the epidermis, then the mesoderm. After stage 12, bib is barely detectable in the embryo.
GBrowse - Visual display of RNA-Seq signalsView Dmel\bib in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
bib function is required autonomously in epidermal precursors to prevent neural development.
The embryonic phenotype of neurogenic mutations was examined in most tissues using Ecol\lacZ enhancer trap lines. All alleles examined show defects in many organs from all three germ layers. At least for ectodermally and endodermally derived tissues, neurogenic gene function is primarily involved in interactions among cells that need to acquire or maintain an epithelial phenotype.
Recessive embryonic lethal, a neurogenic mutant. Homozygotes fail to form ventral, lateral and most of the cephalic epidermis. Central nervous system hypertrophied by recruitment of presumptive epidermal cells, but exhibiting considerable architectural normality. Most epidermal sense organs can be recognized in electron microscope preparations; chordotonal organs prevalent but with abnormal structures, perhaps owing to disrupted attachment.
Loss of bib function approximately doubles the number of neuronal precursors and their progeny cells in the embryonic peripheral nervous system. Mosaic studies reveal a hypertrophy of sensory bristles in bib mutant patches in adult flies, in contrast to results of Dietrich and Campos-Ortega, 1984.
Mutant alleles cause hypertrophy in nau expressing cells, a 2-5 fold increase in nau expressing cells per cluster relative to wild type. The clusters enlarge so much that they merge to form superclusters across the midline.
Ecol\lacZ reporter gene constructs demonstrate that neurogenic loci are required to restrict the number of competent cells that will become sensory mother cells, SMCs.
Mutations of mam, bib and neur in an heterozygous condition had no effect on the expression of NAx-59d or NAx-59b except when coupled in cis with Nfa-g. The neurogenic mutations suppress the wing venation phenotype of N.
Characterisation of bib genomic and complementary DNA suggests the bib product may mediate intercellular communication in a pathway separate from the one involving the products of other neurogenic genes.
Neural hyperplasia, caused by mutations in bib, can be prevented by the presence of another neurogenic mutation.
Effects on central nervous system intermediate with respect to mutations at other neurogenic loci. Insensitive to changes in dosage of other neurogenic genes.
Supernumerary peripheral elements formed by recruitment of presumptive epidermal cells.