mus(2)201, mus-201, ESTS:55A11T , XPG, DmXPG
Gene model reviewed during 5.54
May be component of a dicistronic gene; available data inconclusive (possible low frequency, stage-specific dicistronic transcript).
Gene model reviewed during 5.50
Gene model reviewed during 5.56
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mus201 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\mus201 in GBrowse 2
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: mus201 CG10890
Source for merge of: mus201 ESTS:55A11T
Dicistronic annotation CG32956 split out into separate annotations for each open reading frame, CG13399 and CG10890, in release 4.2 of the genome annotation. CG13399 corresponds to Chrac-14 and CG10890 corresponds to mus201.
Source for merge of mus201 ESTS:55A11T was sequence comparison ( date:000505 ).
Gene is involved in pre-replication DNA repair of UV and AA lesions.
Sex-linked recessive lethal (SLRL) test is used to demonstrate inactivation of the nucleotide excision repair (NER) system has a major impact on mutational response of germ cells to mutagens.
Larval survival hypersensitive to exposure to methyl methanesulfonate, nitrogen mustard and ultraviolet light; weakly hypersensitive to X rays. Female fertility unimpaired and meiotic disjunction regular. Homozygotes devoid of detectable excision repair (Boyd et al., 1982; Dusenbery et al., 1983); postreplication repair and repair of single-strand breaks induced by X rays normal. Hypermutable to alkylating agents (Smith and Dusenbery, 1988). Mutant defect rescued by transformation with the endonuclease V gene (denV) of bacteriophage T4 (Banga et al., 1989).