max, males absent on first, dMOF, males-absent on the X
a MYST family histone acetyltransferase that acetylates His4 at Lysine 16. Mof is part of the male-specific lethal complex that mediates dosage compensation by transcriptional upregulation of the male X chromosome - part of the non-specific lethal complex which regulates expression of housekeeping genes in males and females - regulates DIAP1 and induces apoptosis in a JNK dependent pathway
Please see the JBrowse view of Dmel\mof 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 5.52
3.2 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
827 (aa)
Autoacetylation at Lys-638 is required for binding histone H4 with high affinity and for proper function.
Ubiquitinated by msl-2.
Component of the male-specific lethal (MSL) histone acetyltransferase complex, composed of mof, mle, msl-1, msl-2 and msl-3 proteins, as well as roX1 and roX2 non-coding RNAs (PubMed:10679323, PubMed:11014199, PubMed:16543150, PubMed:18510926, PubMed:20620953, PubMed:20620954, PubMed:22421046). Component of a maternal MSL subcomplex composed of mof, msl-1 and msl-3 (PubMed:32502394). Component of the non-specific lethal (NLS) histone acetyltransferase complex at least composed of mof, nls1, dgt1/NSL2, Rcd1/NSL3, Rcd5/MCRS2, MBD-R2 and wds (PubMed:16543150, PubMed:20620953, PubMed:20620954, PubMed:22723752). In males, interacts with nucleoporin Mtor (PubMed:34133927).
The tudor-knot domain (also named chromobarrel domain) mediates association with roX1 and roX2 non-coding RNAs, promoting recruitment to the male X chromosome (PubMed:11014199). It also potentiates the histone acetyltransferase activity after chromatin binding (PubMed:22421046).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mof using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: maternally deposited
mof transcript is found in larvae and adults of both sexes.
JBrowse - Visual display of RNA-Seq signals
View Dmel\mof in JBrowse1-14
1-15.4
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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 JBrowse 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
The MSL complex does not mediate dosage compensation directly, but rather its activity overrides the high level of histone acetylation and counteracts the potential overexpression of X-linked genes to achieve the proper twofold up-regulation in males.
Gene expression is increased in response to the presence of two copies of Scer\GAL4hs.PB.
Gene products of the male specific lethal (msl) group of genes including msl-1, msl-2, msl-3, mle, and mof are associated with all female chromosomes at a low level but are sequestered to the X chromosome in males. There is evidence for the presence of nucleation sites for association of msl proteins with the X chromosome rather than individual gene binding sites. mof is still capable of associating with the chromosome in msl mutant individuals. It appears to be able to dissociate from other members of the MSL complex under these circumstances and act independently.
Gene products of the male specific lethal (msl) group of genes preferentially associate with the male X chromosome and may have a role in dosage compensation. This may be achieved by regulating an inverse dosage effect, which would be maintained on the male X and nullified on the autosomes.
mof encodes a putative histone acetyl transferase (HAT) that plays a direct role in the specific histone acetylation associated with dosage compensation, the male-specific hypertranscription of X-linked genes. mof function in dosage compensation is supported by the effect of the mutation on the binding of other dosage compensation regulatory factors to the X chromosome and its effect on the normal consequences that this binding has on nucleosomal structure.
Male lethal locus that exhibits a strong maternal effect and is responsible for dosage compensation in males.
Source for identity of: mof CG3025