FB2020_06, released Dec 22, 2020
Gene: Dmel\oc
FB2020_06, released Dec 22, 2020
Gene: Dmel\oc
Gene: Dmel\oc
Gene: Dmel\oc
otd, orthodenticle, Otx, orthodentical, ort
transcription factor - homeodomain - paired-like - acts in a combinatorial fashion with the cephalic gap genes and to assign segmental identities in the head and brain
Please see the JBrowse view of Dmel\oc for information on other features
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Gene model reviewed during 5.44
Gene model reviewed during 5.45
gene_with_stop_codon_read_through ; SO:0000697
Stop-codon suppression (UAG) postulated; FBrf0216884, FBrf0234051.
Gene model reviewed during 6.25
4.7 (northern blot)
671 (aa)
Contains multiple repeats consisting of single amino acids (e.g. Gly, Ser, His, and Asn) and pairs of amino acids (e.g. Gly-Val).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\oc using the Feature Mapper tool.
Comment: reference states 5-13 hr AEL
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
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
In stage 11 embryos, oc transcript is detected in a restricted pattern in the brain. It is absent from the primordia of the pars intercerebralis and pars lateralis.
oc transcripts are expressed at roughly 70-90% egg length in the cellular blastoderm embryo. Beginning at gastrulation, expression retreats from the ventral midline but persists in a major portion of the deuterocerebral and protocerebral neurectoderm forming a horshoe domain that overlaps with the tll expression domain. Expression persists at stage 9 in a broad domain that covers most of the protocerebral domain of the head.
The oc transcript is expressed in a dynamic pattern during embryonic development. Early on, it is expressed in the anterior 20% of the embryo, and the posterior boundary is not well defined. As development proceeds, the posterior boundary of oc expression becomes very well defined and expression begins to receed from the ventral region, and is restricted from the ventral most domain of the embryo. Just before germ band extension, oc expression is restricted from the anterior most region of the embryo and confined to a broad stripe between 5% and 15% egg length. Following germ band extension, oc expression is detected in the procephalic regions and is then detected along the developing ventral midline.
The oc transcript is expressed in a faint broad stipe between 10% and 25% egg length in the anterior region of the cellular blastoderm.
oc transcripts are detected from early embryonic stages until late pupation with the highest levels occurring between 4hr and 13hr of embryogenesis. In cellular blastoderm embryos, oc expression occurs in a broad circumferential stripe at the anterior end of the embryo. After gastrulation, oc expression persists in the procephalic head region and is also seen in cells along the ventral midline.
oc protein is expressed in all photoreceptor cells from the third larval instar onwards, and is maintained throughout photoreceptor cell development.
Starting at embryonic stage 12, oc is expressed in the region of the optic lobe primordium that will give rise to the precursors of the larval photoreceptors and is expressed in all photoreceptors throught embryonic and larval stages.
oc (otd) protein is expressed in a broad domain covering the antennal and ocular segments of embryonic stage 9-11 procephalic neurectoderm. In addition there is a restricted zone of expression in the ventral portion of the procephalic neurectoderm in theintercalary segment and in cells on the dorsal midline of the embryonic head. Expression in procephalic neuroblasts stage 9-11: tritocerebrum - v1; deuterocerebrum - d1-3, d6, v3, v5-6; protocerebrum - ad2, ad4, ad15, ad17, av1, cd1-17, cv2-9, pd1-16, pd18, pd20, pv1-3
GBrowse - Visual display of RNA-Seq signals
View Dmel\oc in GBrowse 21-23
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.
monoclonal
polyclonal
The noc and elB paralogs interact with hth to correctly specify the photoreceptors which detect polarised light at the dorsal rim of the retina, being involved in specifying both morphological and molecular fate. noc and elB also antagonise the transcriptional activator and repressor functions of oc in the retina through distinct protein domains.
Five EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
The primary target genes of Egfr are pnt, vnd and Fas3, these are induced in different ectodermal domains. Secondary target genes oc, argos and trn are activated by pnt in response to Egfr signalling. The proper induction of these genes requires the concomitant inactivation of aop, mediated by Egfr signalling.
High levels of bcd morphogen are not required for oc activation. The terminal system contributes to oc activation in the head primordium. Repression of oc expression at the anterior terminus of the blastoderm is mediated by hkb and requires input from all three maternal morphogens that specify embryonic head development.
hh and wg specify the identities of specific regions of the head capsule. During eye-antennal disc development hh and wg expression initially overlap, but subsequently segregate. This regional segregation is critical to head specification and is regulated by oc. oc is a candidate hh target gene during early eye-antennal disc development.
Most metazoan homeodomains share a preference for the TAAT motif, they can differ from each other in their preference for the bases immediately 3' to this core. This preference is determined, in part, by the identity of amino acid position 50. Because homeodomain sequences have been identified that possess at least 10 different amino acids at position 50 it is investigated whether multiple DNA binding specificities can be conferred by changing this position to a variety of amino acid side chains.
oc is required for photoreceptor cell development in the developing eye.
Activation of cnc in intercalary and mandibular primordia requires zygotic gap gene products, activation by btd and repression by oc (anteriorly) or sna (ventrally).
Superunstable mutations generated in crosses of π2 strain to a wa strain or its derivatives. Each superunstable mutation gives rise to a large family of new super-unstable mutations with a wide range of phenotypic expression. Mutations with the same phenotype often differ in the specificity of their potential for further mutation. Each superunstable mutation is associated with a specific, "paired", reversible mutation. Active transposase encoded by P elements is necessary to maintain superinstability. X transposable element is also implicated in the mutability system.
The requirement for oc during postblastoderm stages has been studied.
oc has a gap-gene-like role in mediating the development of head structures. In oc mutant embryos the posterior border of gt stripe 1 and all of stripe 2 are shifted posteriorly. oc is positively regulated by bcd.
Mutations in zygotic gene oc interact with RpII140wimp.
btd, ems and oc are required to establish contiguous blocks of segments and may behave like gap genes that mediate bcd function in the embryonic head.
Molecular and phenotypic characterization of oc indicates that oc is necessary for the formation of the CNS.
A number of super-unstable mutations at the oc locus have been studied.
Mutagenesis in strains carrying unstable mutations at the oc locus has been studied.
One mutation in oc is due to insertion of a Stalker element.
A screen for X-linked genes that affect embryo morphology revealed oc.
oc mutants display anterior denticle belts pointing posteriorly, defects at the ventral midline and head defects.
Relationship of oc to otd indicated by co-mapping (cf. Spradling and Mahowald, 1981; Wieschaus et al., 1984) and the failure of otd-type alleles to complement oc (Finkelstein et al., 1990). Moreover, otd/+ females have altered adult bristle pattern in ocellar region, similar to that exhibited by homozygotes for the weak allele ocdb (Finkelstein, Smouse, Capaci, Spradling and Perrimon, 1990).
Ocelli completely absent. Bristles in ocellar area and on top of head irregular and more numerous; postverticals usually absent. Eyes somewhat reduced and body size dwarfed. Phototaxis normal (Benzer, 1967). Viability about 90% wild type. oc and deficiencies for oc show partial dominance to oc+; ocelli placed somewhat far back on head and slight indentation apparent between postvertical bristles (Craymer and Roy, 1980). Ubl/+ enhances dominance of oc; Df(1)RA2/+ exhibit delayed hatch and an oc phenotype; oc2/+ display strong oc phenotype and oc1/oc1 are lethal in combination with Ubl/+ (Mortin and Lefevre, 1981). Lethal alleles (recovered as otd: orthodenticle) die as embryos; all denticles in anterior abdominal segments point posteriorly; defects at ventral midline; head defects. Also cause embryonic neural defects (Finkelstein, Smouse, Capaci, Spradling and Perrimon 1990): In developing ventral cord, commissures within each segment appear fused. At the cellular level, certain ventral unpaired medial (VUM) neurons do not seem to migrate ventrally (as do the normal VUMs at approximately 14 hours of embryogenesis) and are absent from most segments. Other 'midline-associated' neurons are missing as well in otd-type embryos. Homozygous germ-line clones survive in females; homozygosity for lethal alleles in germ-line clones without effect on survival of heterozygous offspring or on phenotype of hemizygotes (Wieschaus and Noell, 1986). Putative oc transcript abundant in embryos, peaking between 4 and 13 hours, before and coincident with neural-developmental defects observed in central nervous system of embryos hemizygous for lethal alleles; there is also putative maternally derived oc mRNA (which could be alternately spliced form of the 'major' transcript). Northern signals weaken in L1 and L2, are still detectable in early pupae, but are absent in late pupae and adults. In situ hybridization reveals earliest embryonic expression at cellular blastoderm; later, signals seen in a longitudinal strip along ventral midline, then in 'head region' and in developing ventral cord.
