Ba, l(2)01092, Brista, Distall-less
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.52
A non-AUG start codon may be used for translation of one or more transcripts of this gene; based on the presence of conserved protein signatures within the 5' UTR without an in-frame AUG (FBrf0243886).
3.4, 2.5 (northern blot)
None of the polypeptides share 100% sequence identity.
327 (aa)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Dll using the Feature Mapper tool.
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 larval eye primordium
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
Comment: reported as ventral imaginal precursor specific anlage
Dll is normally expressed in the imaginal limb primordia of segments T1, T2, and T3 in embryos. In BXC- embryos, expression is also seen in ectopic primordia in segments A1-A9.
Dll transcripts are detected initially in post blastoderm embryos and are present at increased levels during late embryogenesis. They are also expressed in all three larval instars with the lowest level in 2nd instar. Later stages were not tested.
Dll is expressed in the embryonic precursors of the dorsal organ (antennal primordium) and terminal organ (maxillary sensory complex primordium), continuing into those organs through the third larval instar. During sense organ specification, Dll protein is coexpressed with the proneural transcription factor ato and sense organ transcription factor sens in subsets of sensory organ precursors in the head segments. By embryonic stage 16, sens is expressed in the ganglia of the dorsal organ, terminal organ, and ventral organ, as well as in some of the eo support cells (thecogen, tormogen, and trichogen cells).
Dll expression was compared in the wing and haltere discs. Expression is present along the D/V axis in wing but not haltere.
Dll protein is detected in third instar larval antennal discs in the primordia of antennal segments 1, 2 and 3 and in the arista primordia.
At embryonic stage 11, Dll is expressed in a group of cells straddling the anterior/posterior compartment boundary of the thoracic hemisegments, as well as in the segments of the head.
GBrowse - Visual display of RNA-Seq signals
View Dmel\Dll in GBrowse 22-107
2-111.7
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.
Source for identity of: Dll CG3629
Source for merge of: Dll BcDNA:LP01770
Source for merge of Dll BcDNA:LP01770 was a shared cDNA ( date:030728 ).
Haploinsufficient locus (not associated with strong haplolethality or haplosterility).
DNA-protein interactions: genome-wide binding profile assayed for Dll protein in 0-12 hr embryos; see mE1_TFBS_Dll collection report.
Nonsense-mediated mRNA decay (NMD) down-regulates a distinct splice isoform(s) of this gene.
Patterns of canalization and trait correlation have been examined using Dll11 and high temperature stress on a panel of iso-female lines.
Dll may restrict expression of proximal-leg specific gene expression.
Genetic combinations with mutants of nub cause additive phenotypes.
Dll has two separate functions: a primary function to induce the formation of ventral appendages and their identity, and a secondary function involved in the differentiation of the wing margin pattern.
A technique using fluorescent probes to detect a mRNA and a protein simultaneously in the embryo is used and results suggest Dll-driven expression of a Ecol\lacZ reporter gene is activated in the ventral region of the limb primordia and Dll-positive cells migrate from a ventral position to a dorsal one within a single limb primordia.
Dll is required for proximal-distal axis formation in the limbs.
Comparison of Dll and wg expression in Drosophila and the butterfly P.coenia suggests a common mechanism underlying the formation of all insect appendages. The limb-type-specific patterns of Dll expression indicate that the regulation of Dll expression may be critical to limb morphology, and are inconsistent with Dll functioning in a simple distal-to-proximal concentration gradient.
Dll and Dfd are both persistently expressed in ventral maxillary cells, and combinatorially specify a subsegmental code required for a group of cells to differentiate maxillary cirri. The regulatory effect of Dfd on Dll is mediated by a ventral maxillary-specific enhancer located 3' to the Dll transcription unit.
Null alleles are recessive embryonic lethals, with dominant developmental defects of distal appendages. Lethal embryos lack certain sensilla, including Keilin's organs and antennal, maxillary, labial and labral sense organs, all of which are thought to correspond to vestiges of the distal sensilla of rudimentary larval appendages. No other embryonic sensilla are affected, nor are the neurons innervating the rudimentary appendages detectably abnormal. In homozygous-viable or pharate-adult-lethal hypomorphic alleles defects are found in all appendages represented by the above larval structures. Heterozygotes for lethal alleles are characterized by transformations of distal antennal segments (i.e., AII, AIII and arista) to mesothoracic leg and by variable loss of distal leg segments, depending on severity of allele. Transformation in the case of Dll1 sensitive to low-temperature pulses throughout larval development, whereas the TSP for leg truncation is at end of the third larval instar. Clones of homozygous Dll- cells incapable of contributing to any but the coxal segment of the legs and for the most part, the first antennal segment; in the relatively infrequent cases, in which Dll- clones involve distal antennal segments, Dll- portions, which always include at least the arista, are absent and Dll+ portions develop normally indicating cellular autonomy.
A minimal cis-regulatory enhancer element, Dll-304, directs Dll expression in larval leg primordia. Bithorax complex proteins repress Dll expression in abdominal segments by binding to a small number of specific sites in the element, and mutating the sites eliminates binding of bithorax complex proteins and renders the element insensitive to their regulation.
Limb development depends specifically on Dll gene activity.
Homeotic gene activity programs primordia as either discs or histoblast nests by the early extended germ band stage.
Dll plays an important part in specifying proximo-distal positional information.
Dll activity is required for the distal domains of the adult limbs: legs, labial palps, maxillary palps, antennae and clypeolabrum.
Dll acts as a developmental switch that is required to promote the development of limb structures.