mus(1)101, fs(1)K451, mus-101, TOPBP1
Gene model reviewed during 5.39
Gene model reviewed during 5.45
There is only one protein coding transcript and one polypeptide associated with this gene
1425 (aa); 158 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mus101 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\mus101 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.
Gene is involved in post-replication translesion synthesis repair.
Mutations in mus101 reduce chorion gene amplification.
Mutations of mus101 disrupt late oogenesis and affect normal amplification of all chorion genes.
Survival of homozygous and hemizygous larvae hypersensitive to exposure to methyl methanesulfonate, nitrogen mustard, 2-acetylaminofluorene and gamma rays. Partially deficient in post-replication repair (Boyd and Setlow, 1976; Brown and Boyd, 1981); nitrogen-mustard mutagenesis abolished; mus101+ implicated in recovery from DNA crosslinking (Graf, Green and Wurgler, 1979). Displays hypermutability to alkylating agents; defective in alkylation repair pathway (Smith and Dusenbery, 1988). Increases X-ray-induced post-meiotic chromosome loss (Cooper and Zimmering, 1981). Mutants inhibit premeiotic rDNA magnification in males (Hawley, Marcus, Cameron, Schwartz and Zitron, 1985). mus101 function required for chorion-gene amplification (Snyder, Galanopoulous and Kafatos, 1986). Homozygotes for female-fertile allele exhibit elevated meiotic nondisjunction (Boyd et al., 1976). Causes mitotic chromosome instability (mus101D1, Baker and Smith, 1979), and defective mitotic condensation of heterochromatin (mus101ts1, Gatti et al., 1983).