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FB2026_01
,
released March 12, 2026
l(1)114, 114, l114, M67
secreted - novel protein - regulates gastrulation via GPCRs - necessary for coordination of cell shape changes throughout the invaginating primordia - regulates motor axon guidance, glial organization and morphogenesis
Please see the JBrowse view of Dmel\fog for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.53
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.46
Gene model reviewed during 5.56
3.7 (longest cDNA)
730 (aa)
May be highly O-glycosylated in its Ser/Thr-rich C-terminal part.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\fog using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
fog transcripts are detected in the wing disc folds and in the wing pouch.
The pattern of fog transcription precisely precedes the pattern of apical constrictions in the ventral furrow and in the posterior midgut primordia. Zygotic fog transcription begins in the ventral furrow primordium during the beginning of cellularization, about 30 min. before the start of constrictions. The region of fog transcription encompasses a 12-14 cell wide region of the mesoderm primordia. This corresponds to the subset of ventral furrow cells that make up the initial invagination. During invagination, fog transcripts disappear rapidly from the furrow. fog is also expressed in the invagination primordia of the posterior midgut before invagination begins and disappear as the invagination closes.
The fog protein is secreted.
JBrowse - Visual display of RNA-Seq signals
View Dmel\fog in JBrowsePlease Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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 JBrowse 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.
Loss of fog promotes mitochondrial fusion.
fog signal is both necessary and sufficient to trigger the relocalisation of myosin to the apical side of the cell.
New annotation (CR41108) in release 3.2 of the genome annotation. New annotation (CR41109) in release 3.2 of the genome annotation. New annotation (CR41110) in release 3.2 of the genome annotation.
Activation of the fog/cta pathway results in ectopic cell shape changes in the gastrula. The normal location of the ventral furrow in embryos with uniformly expressed fog suggests the existence of a fog-independent pathway determining mesoderm-specific cell behaviours and invagination. Epistasis experiments indicate this pathway requires sna but not twi expression.
The fog gene product is required during gastrulation for two morphogenetic movements, formation of the ventral furrow and invagination of the posterior midgut primordium, and coordinates cell shape changes by inducing apical constriction of cells in a spatially and temporally defined manner. The maternal contribution of fog product can supplement but not substitute for the zygotic activity. Over-expression of fog can induce ectopic constrictions, and hasten the onset of posterior midgut invagination. fog seems to function as a secreted signal that activates the G protein α subunit encoded by cta in neighboring cells.
In fog mutant embryos the early constricting cells in the ventral furrow are scattered throughout most of the mesoderm primordium. As a result of the reduced number of appropriate cell shape changes the ventral furrow invaginates later than wild type and with a much less regular appearance.
Muscle phenotype of mutants studied using polarised light microscopy and antibody staining to detect Mhc-lacZ reporter gene expression in muscles.
Hemizygous lethal; the cellular blastoderm apparently normal and gastrulation begins at normal time. No posterior midgut formed; germ band does not elongate onto dorsal side of embryo but it is thrown into a series of transverse ventral folds. Older embryos often twist around the longitudinal axis for one complete turn; many exhibit an anterodorsal hole through which the brain protrudes and a split in the posterior CNS and protrusion of the midgut. Hemizygous deficiency gives same phenotype. No effect of maternal genotype; homozygous germ line clones make eggs capable of supporting normal embryonic development. Fate mapping localizes fog lethal focus to the posterior pole most likely in presumptive posterior-midgut or proctodaeum cells.
Zygotically active locus involved in the terminal developmental program in the embryo.
Mutations in fog block the transition from the first slow stochastic phase of gastrulation to the second rapid phase of constriction in the ventral furrow and the posterior midgut invaginations.
fog mutants display defective gastrulation, extensive folds in the germ band and ventral holes in the cuticle particularly at the anterior and posterior end.
Source for merge of: fog CR41108 CR41109 CR41110
Annotations CG9559, CR41108, CR41109 and CR41110 merged as CG9559 (which corresponds to fog) in release 4.3 of the genome annotation.
