Secretion enhancer-binding protein 2, Sebp2
winged-helix nuclear transcription factor - plays two roles in the formation of the embryonic salivary glands: an early role in promoting survival of the secretory cells, and a later role in secretory cell invagination works with bHLH protein Sage to activate expression of salivary gland specific gene products, such as secreted proteins and their modifying enzymes
Please see the GBrowse view of Dmel\fkh or the JBrowse view of Dmel\fkh for information on other features
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Gene model reviewed during 5.55
Gene model reviewed during 5.44
Double stop-codon suppression (UGA, UAA) postulated; FBrf0216884,
gene_with_stop_codon_read_through ; SO:0000697
Gene model reviewed during 5.40
Gene model reviewed during 6.02
4.2 (northern blot)
510 (aa); 54 (kD)
fkh protein is used as a marker for the epithelium of the foregut and hindgut primordia.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\fkh using the Feature Mapper tool.
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as salivary gland body specific anlage
Comment: reported as large intestine specific anlage
Comment: reported as rectum specific anlage
Comment: reported as salivary gland primordium
Comment: reported as small intestine specific anlage
Expression assayed at stages 9, 11, 13, and 17. Expression may be continuous between assayed stages in some tissues.
fkh transcripts are detected in blastoderm embryos in the terminal domains from 0-15% egg length and from 95-100% egg length.
Comment: ectodermal cells
fkh protein gradually disappears from the salivary gland nuclei, but remains strong in the imaginal rings that will later form the adult salivary gland.
fkh protein is used as a marker for the epithelium of the foregut and hindgut primordia.
fkh protein is expressed in the ectodermal cells of the developing embryonic foregut. Expression stops sharply at the ectodermal/endodermal boundary.
fkh protein isdetected shortly after the onset of fkh transcription. It is firstdetected in the posterior domain at the end of the syncytial blastodermstage and in the anterior domain at the beginning of the cellularblastoderm stage. By the end of cellular blastoderm, the expressiondomains cover 0-13% egg length and 94-100% egg length. Double stainingwith the ftz antibody indicates that the posterior domain covers theregion posterior to parasegment 15. Subsequently, the anterior domain ofexpression expands such that by germ band elongation it covers theanterior midgut and stomodeal primordia. Yolk nuclei also stain. Later, itis expressed in the developing salivary glands and in the CNS.
GBrowse - Visual display of RNA-Seq signals
View Dmel\fkh in GBrowse 2
3-96
Please 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 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.
polyclonal
fkh protects the salivary glands from hormone-induced death until a stage-specific, hormone-induced loss of the protein earmarks the tissue for destruction in response to future hormone exposure.
fkh has at least two roles in the formation of embryonic salivary glands; an early role in promoting survival of secretory cells and a later role in secretory cell invagination, specifically in the constriction of the apical surface membrane.
In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.
Mutants are isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis: mutants exhibit gap pattern defects.
cad acts in hindgut development through fog, fkh and wg, but does not play a role in activating tll, hkb, byn and bowl which are also required for proper hindgut development. cad, fkh, byn and wg constitute a conserved constellation of genes that plays a required role in gastrulation and gut development.
The distinction between pregland and preduct cells is made by the combination of two spatially separated negative regulatory steps: the Egfr signaling pathway represses fkh in the preduct cells and fkh represses duct specific genes in the pregland cells. trh is a duct-specific gene activator and is one of the targets of fkh repression.
fkh is required for stomodeal nervous system development.
The organisation of the tail region of the embryo is documented from studies of cuticular markers enabling a more direct comparison between homologous structures on the embryo and larval cuticle.
In salivary gland development the activity of fkh prevents the expression of duct-specific cells, and in preduct cells the spi group signalling pathway prevents the expression of gland specific markers. fkh is repressed by spi group signalling, which is strongest in the most ventral cells of the epidermis.
Identified by virtue of their products binding the Sgs4 regulatory region in a mobility shift assay.
Co-crystal structure of the HNF-3/fork head DNA-recognition motif resembles histone H5.
Seven genes isolated by low stringency hybridization to a probe containing coding sequences for fkh domain conserved in the rodent hepatocyte enriched nuclear transcription factor. All seven genes include a 110 amino acid conserved sequence, overall amino acid identity varies between 45% and 62%, and two are accounted for by the two slp genes slp1 and slp2. The remaining five are fd59A, fd64A, fd78E, fd96Ca and fd96Cb.
fkh is highly homologous to the rat hepatocyte nuclear factor-3 gene family.
Zygotically active locus involved in the terminal developmental program in the embryo.
fkh mutants exhibit transformation of nonsegmental terminal regions into segmental derivatives, especially deletions of hindgut and Malpighian tubules.
A sequence comparison between fkh and the rat HNF-3A gene suggests the existence of a new class of transcription factors that is conserved between Drosophila and mammals. The name "fork head" domain is suggested for the characteristic DNA binding motif.
A number of cis regulatory elements within the genomic DNA of the fkh gene have been identified.
The molecular identification, structure and expression pattern of the fkh gene product demonstrate that it is localized in the nucleus and may act as a transcriptional regulator.
fkh is required in the very anterior and posterior ectodermal regions of the embryo. Inactive fkh causes homeotic transformations, the appearance of post-oral head structures in the terminal domains. There is no morphological evidence for the expression of fkh in the cells of the female germ line. Mitotic recombination demonstrates that fkh is not required in a cell autonomous manner for normal development of the imaginal discs.
fkh mutants display a forked head skeleton and no anal pads.
Embryonic lethal. fkh+ appears to be required in the most anterior and posterior regions of the embryo; in amorphic mutants homeotic transformation effects the appearance of post-oral head structures in these terminal domains. The ectopic head structures are sometimes associated with thoracic structures anteriorly and anterior tail structures posteriorly. Thus fkh mutations produce transformations directed to the center involving structures normally found in different parasegments. Anteriorly, esophagus and proventriculus, derivatives of the ectodermal stomodaeum, are absent but not the pharynx or the hypopharyngeal organ, which resides on the anterior surface of the embryo; parts of the head skeleton are distorted; other parts apparently normal. Salivary glands absent. Posteriorly, anal pads and Malpighian tubules, derivatives of the ectodermal proctodaeum, are absent; replaced by anterior tail structures and post-oral head structures; supernumerary anal sensilla and dorsal hairs also present. Anterior and posterior fkh domains are beyond the regions controlled by ANTC and BXC, respectively; however ectopic expression of ANTC and BXC expression can occur in the fkh domains of fkh but not fkh+ embryos. No maternal effect. Homozygous fkh clones in adult cuticle completely normal in structure indicating no requirements for fkh+ in imaginal disk development. In situ hybridization reveals transcript in two terminal domains shortly before blastoderm cellularization occupying 5% embryonic length anteriorly and 15% posteriorly. fkh protein first detected in posterior domain at the end of syncytial blastoderm and the anterior domain at the beginning of cellularization. Expression continues in the derivatives of the ectodermal stomodaeum and proctodaeum throughout gastrulation. In addition fkh protein is detected in the midgut, the salivary glands, the central nervous system and the yolk cells.
