fli, flightless, W2, fltO, l(1)W-2
Gene model reviewed during 5.49
There is only one protein coding transcript and one polypeptide associated with this gene
Consists of a leucine-rich N-terminal half, which is likely to be involved in protein-protein interaction, and a C-terminal half which has high sequence similarity to gelsolin and is therefore likely to be involved in actin-binding.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\fliI using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\fliI 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.
Source for identity of: fliI CG1484
Source for merge of: fliI BcDNA:LD21753
Source for merge of fliI BcDNA:LD21753 was sequence comparison ( date:990717 ).
Allelism tests with flt mutants not carried out.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Maternally synthesized fliI is required for the proper distribution of actin along the membrane network and for cellularisation to proceed properly.
Molecular analysis of fliI indicates that a region of the S1-like domain of the molecule implicated in the binding of a calcium ion in gelsolin may be responsible for the observed flightless phenotype of the mutant.
fliI gene locus has been molecularly cloned and the gene product characterised.
fliI was involved in a study of the base of the X chromosome: genetic and germline clone analysis.
Mosaic analysis suggests primary defect in thoracic muscles.
Viable and lethal alleles have been isolated. Viable alleles are recessive and flightless; wing position normal; jumping abilities variously impaired depending on allele. Temperature-sensitive alleles show temperature-sensitive period to be during first half of pupal stage. Indirect-flight-muscle fibers are wavy with amorphous internal structures; myofilaments disorganized; Z bands and myofibrils abnormal; thin filaments often aggregated into bundles with striations (not seen in wild type). Lethal alleles die in larval or pupal stages. Maternal effect lethal; progeny produced from homozygous female germ-line clones of severe alleles (e.g., fliI14) are not rescuable by normal allele of paternal origin; abnormal folding during gastrulation; mesoderm invagination abnormal; only patches of epidermis present at later stages; embryos from clones homozygous for weaker alleles (e.g. fliI22) were more nearly normal in appearance.