l(3)05592, ms(3)61CD, gov, Ach, extramacrochaete
transcription factor - HLH non basic - antagonist of proneural genes - the Notch pathway is required in combination with Emc to define the proneural cluster which gives rise to the sensory organ precursor cell
Please see the JBrowse view of Dmel\emc 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.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.45
2.5 (northern blot)
4.1, 2.3, 1.85, 1.7 (northern blot)
2.0 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
199 (aa); 22 (kD predicted)
199 (aa)
Heterodimers between the da protein and either the ac, sc, or l(1)sc proteins were found to bind specifically to E box consensus sequences in the ac promoter region in vitro. The three heterodimers had differing affinities for the E boxes acE1-acE3 and none bound to acE4. This binding was inhibited in a concentration dependent manner by the emc protein. emc did not inhibit sequence specific DNA-binding by the mouse CREB transcription factor showing that it is not a general antagonist of DNA binding.
emc protein contains the dimerization domain of other helix-loop-helix proteins but lacks the basic region thought to be important for DNA binding. It is thought to form heterodimers with other bHLH proteins and interfere with their activity.
emc contains a helix-loop-helix region but lacks the basic domain thought to be important for DNA-binding. It is thought to sequester proneural proteins in complexes inefficient for DNA interaction.
Heterodimer with other HLH proteins.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\emc using the Feature Mapper tool.
Comment: maternally deposited
Comment: anlage in statu nascendi
Comment: 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: reduced at the morphogenetic furrow
emc expression is reduced in the region of the morphogenetic furrow but is otherwise uniform in eye discs from third instar larvae.
emc is expressed ubiquitously in oogenesis stages 1-6 in the follicle cells and in the nurse cell cytoplasm. Subsequently, expression becomes restricted to a tight band of follicle cells at the nurse cell-oocyte boundary and to the stretched follicle cells over the nurse cells at stage 10A and 10B. During stage 11, expression is refined to two subsets of follicle cells either side of the dorsal midline. Expression persists in these follicle cells as they migrate anteriorly, secreting the dorsal appendages, but becomes expressed in a single large area covering the dorsal midline. By stage 14, expression is limited to a small group of folicle cells located between the dorsal appendages.
Comment: absent from the morphogenetic furrow
emc protein expression is absent from the morphogenetic furrow but is otherwise relatively uniform in eye discs from third instar larvae.
emc protein is detected by immunolocalization in follicle cells at all stages of oogenesis. Expression is not very strong at stage 7-8. It is present in all germline cell nuclei in middle and late oogenesis (stages 8-13), in the centripetal cells at stage 10 and in the posterior pole cells (stage 10,11). At stages 11-12, emc is expressed in two dorsal anterior subsets of follicle cells on either side of the dorsal midline. During stage 12, these dorsal folicle cells migrate anteriorly and at stage 13, emc is only detected in the follicle cells of the developing dorsal appendages.
GBrowse - Visual display of RNA-Seq signals
View Dmel\emc in GBrowse 2
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: emc CG1007
Source for merge of: emc ms(3)61CD
emc is required during development of the imaginal wing discs in both cell proliferation and cell differentiation processes.
Candidate gene for quantitative trait (QTL) locus determining bristle number.
Mutations show strong interactions with high and low selection lines, abdominal and sternopleural bristle numbers are affected. Results suggest emc is a candidate for bristle number quantitative trait loci (QTL) in natural populations or is in the same genetic pathway.
Five additional alleles have been derived by Δ2-3 mobilization of P{lArB} during an analysis of quantitative trait loci effects on bristle number.
emc and h are expressed ahead of the morphogenetic furrow, emc has only a minor function in normal eye development. In emc- h- clones the morphogenetic furrow and differentiated eye field advance up to eight ommatidial rows ahead of adjacent wild type tissue. Results indicate that the morphogenetic furrow and neuronal differentiation are negatively regulated by a combination of anteriorly expressed HLH regulatory proteins, emc and h function together to regulate timing of furrow progression and photoreceptor development.
Clonal analysis demonstrates the emc gene participates in the control of cell proliferation within inter-vein regions in the wing. Similar effects are seen in the haltere and the leg. Behaviour of emc cells indicates that proliferation is locally controlled within intervein sectors, cells proliferate according to their genetic activity along preferential positions in the wing morphogenetic landscape and cell proliferation in the wing is integrated by 'accommodation' between mutant and wild-type cells.
emc is required for a variety of developmental processes occurring in derivatives of the three embryonic germ layers.
emc transcript is maternally contributed and distribution of emc transcripts during embryonic development is determined. emc function is required for normal midgut and Malpighian tubule development. Results suggest that negative regulation by emc may be a common feature of developmental processes involving da the AS-C and possibly other helix-loop-helix proteins.
Mutants display hyperplastic phenotype, tissue overgrowth in mitotic recombination clones.
Postmeiotic differentiation defect.
emc contributes to sensory organ positioning in the wing disc.
Direct, positive transcriptional autoregulation by the ac protein and cross-regulation by sc are essential for high level expression of the ac promoter in the proneural cluster. These auto- and cross-regulatory activities are antagonized in a dose-dependent manner by the emc gene product, whose expression pattern in wing discs is complementary to that of the proneural genes.
Negatively regulates sc expression, probably by interfering with activators of the gene.
A synergistic interaction is observed between E(spl) and emc alleles with regard to the ectopic posterior macrochaetae. emc+ exerts its function by repressing ASC functions and consequently modifying the time and place where sensory organ mother cells are singularized. The NAx-1, NAx-M2 and NAx-M3 alleles reduce the phenotype of emc alleles.
Negative regulator that suppresses sensory neurogenesis by selectively repressing ac and sc gene expression in different spatial domains and at different developmental stages.
Lack-of-function alleles of emc exaggerate Hw phenotypes in both ectopic and normal positions.
DNA sequence analysis reveals four E box binding sites, for the binding of hetero-oligomeric complexes composed of da or AS-C proteins, in the first 877 bp of the ac upstream region. Electrophoretic mobility shift assays demonstrate that the emc protein can specifically antagonise DNA binding of the da/AS-C complexes in vitro in a dose-dependent manner, h and E(spl) proteins fail to exhibit this inhibitory effect.
Mutations in emc cause extra longitudinal or transverse veins with plexated vein phenotypes. Px, px, net, dsr and emc belong to the same synergistic group and act synergistically against kn, fu and shf.
emc has been cloned and characterised.
emc encodes a protein with a helix-loop-helix domain, but lacks a basic region (which is presumably important for DNA binding).
Px, net, dsr, px and emc loci belong to the plexus phenotypic group within the 'excess-of-vein' mutant class. Extra veins occur parallel to and between normal veins that connect to each other by crossveins, forming plexi. Plexi are distal. Proximal regions shift to the margin leaving a central area devoid of veins. Sensilla and chaetae appear shifted. Combinations of mutations produce superadditive phenotypes.
A negative regulator of ac and sc transcription.
Genetic mosaic analysis demonstrates that emc is involved in cell to cell interaction process and patterning of the wing veins.
emc and sc mutants were used to study how different levels of sc expression affect the pattern of chaetae.
Hypomorphic alleles, or amorphic alleles when heterozygous with a hypomorphic allele, cause formation of extra macrochaetae. Severely hypomorphic combinations also cause formation of extra microchaetae. Amorphic alleles when homozygous result in embryonic lethality. Amorphic alleles when heterozygous with a normal third chromosome result in the appearance of ectopic chaetae in the occipital and premandibular regions. Extra chaetae in emc mutant flies appear on the head and notum (weak alleles) as well as on the wing blade, pleura, post-scutellum, tergites and legs in more severe allelic combinations. In severely hypomorphic allelic combinations extra campaniform sensilla occasionally appear on the wing blade. Reduction of wild-type emc function also causes the presence of extra bits of wing vein. A dominant emc allele (emcD) causes a reduction in the number of macrochaetae on the head and notum. emcD is homozygous viable; emcD homozygotes are more mutant than emcD/+ individuals. The L4 and L5 wing veins are shortened in emcD homozygotes but only rarely in emcD/+ heterozygotes. The insufficiency produced by emc can be titrated by altering the dosage of ASC; increased function of ASC produced by gain-of-function mutations (Hw) can be titrated by altering the dosage of emc+.
