dMyc, dm, diminutive, d-myc, c-Myc
bHLH - leucine zipper - homologous to vertebrate Myc proto-oncogenes - controls cell cycle progression, cell growth, cell competition and regenerative proliferation - suppresses tumor invasion and cell migration by inhibiting the JNK signaling
Please see the JBrowse view of Dmel\Myc for information on other features
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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.
Gene model reviewed during 5.53
Gene model reviewed during 5.45
Tissue-specific extension of 3' UTRs observed during later stages (FBrf0218523, FBrf0219848); all variants may not be annotated
Gene model reviewed during 5.55
Shares 5' exon(s) with downstream non-coding gene; shared promoter.
6 (northern blot)
717 (aa)
Efficient DNA binding requires dimerization with another bHLH protein (PubMed:8929412). Binds DNA as a heterodimer with Max (PubMed:8929412). Interacts with ago (PubMed:15182669, PubMed:24173801). Interacts with lid (PubMed:17311883). Part of a complex containing lid, Myc and ash2 (PubMed:17311883). Component of a complex with pont and rept (PubMed:16087886). Interacts with puf (PubMed:24173801).
Probably targeted for ubiquitination by the SFC ubiquitin ligase complex member ago, leading to its proteasomal degradation.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Myc using the Feature Mapper tool.
Comment: maternally deposited
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: 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 in statu nascendi
Comment: reported as salivary gland body specific anlage
Comment: reported as anal pad specific anlage
Comment: 72-76 hours AEL
Myc is ubiquitously expressed in second instar larval wing discs, and then intensifies at the wing hinge in early third instar larvae.
In wandering third instar larvae, Myc expression intensifies in the dorsal mesothoracic tergum (notum) primoridum and in the wing pouch, but is restricted from the anterior-posterior compartment boundary of the wing disc.
Expression at embryonic stage 5 is observed in an anterior stripe. Expression at embryonic stages 10-11 is observed in the ectoderm and in the developing optic lobes. Expression at embryonic stages 13-16 is observed in the midgut.
expression of dm in the eye disc is at low levels, with a stronger stripe immediately posterior to the morphogenetic furrow.
The dm transcript is detected at higher levels in early embryos and in adult females, and at very low levels in larvae and pupae. Additional transcripts of smaller sizes are found in early embryos and in adult females. In situ hybridization experiments reveal that the dm transcript is at first ubiquitous in early embryogenesis, but that it subsequently becomes concentrated in anterior and posterior regions. During gastrulation, additional dm expression is detected in the presumptive mesoderm, along the ventral midline. The mesodermal expression of dm intensifies at germ band extension, and continues through late embryogenesis. The anterior and posterior staining follow the anterior and posterior midgut primordia through extended germ band stages. dm is also transiently detected in salivary gland placodes. dm is expressed in mitotically dividing, as well as in endoreplicating, tissues. During oogenesis, dm transcript is detected in the germarium and at lower levels in stage 1 and stage 2 egg chambers. From stage 3 onward, dm is detected in all cell types of the eggchamber.
Comment: 72 hours AEL
At 72 hours after egg laying (AEL), expression of Myc transiently overlaps with expression of wg in hinge cells and inner ring of the wing disc. In wandering third instar larvae, Myc is expressed in the dorsal mesothoracic tergum (notum) primoridum and in the wing pouch, but is restricted from the anterior-posterior compartment boundary of the wing disc.
Myc is highly expressed in stem cells and cystoblasts but is downregulated in 16-cell cysts.
GBrowse - Visual display of RNA-Seq signals
View Dmel\Myc in GBrowse 2Please 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: Myc dm
Source for merge of: dm anon-WO03040301.171
Source for merge of: dm l(1)G0354 l(1)G0359
Changed from 'dm' ('diminutive') to 'Myc' to reflect preferred usage in the Drosophila literature and facilitate access to information on this gene for naive/non-Drosophila researchers.
"l(1)G0354" may affect "dm".
Source for merge of dm anon-WO03040301.171 was sequence comparison ( date:051113 ).
"l(1)G0359" may affect "dm".
dm expression stimulates glycolysis but impairs oxidative phosphorylation.
S2 cells transfected with dsRNA made from templates generated with primers directed against this gene show a slowing down in G1 phase and a decrease in cell size in all phases of the cell cycle.
Targets for transcriptional regulation by the dm product are characterized by the presence of an E-box, typically within the first 100 nucleotides of the promoter.
RNAi generated by PCR using primers directed to this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
dm plays an essential role in promoting the rapid growth that must occur in both the germline and the surrounding follicle cells for oogenesis to proceed.
dm regulates organ size by inducing cell competition.
Loss of function mutations cause a growth disadvantage. Over-expression causes a growth advantage. Neither loss of dm nor its overexpression causes pattern abnormalities.
Myc is isolated from an embryonic library by interacting with mouse MaxΔ9 bait protein in the yeast two-hybrid assay. The ability of P-element-mediated ectopic expression of Myc to reverse a subset of the phenotypic alterations associated with the dm mutation suggests that dm may correspond to Myc. This finding, along with the localisation of Myc expression to zones of high proliferative activity in the embryo, implicates Myc as an integral regulator of growth and development.
The product of dm has been isolated as a binding partner for human Max in a two hybrid library screen.
Nichols-Skoog, 9th Oct. 1933.
Named 'Myc' after the human ortholog.