Disease relevance of mus101

• The mutagen-sensitive-101 (mus101) gene of Drosophila melanogaster was first identified 25 years ago through mutations conferring larval hypersensitivity to DNA-damaging agents [1].

High impact information on mus101

• The data suggest that the mutagen-sensitive and repair-defective phenotypes of viable mus-101 mutants result from a disruption in chromosome organization [2].
• Other alleles of mus101 causing different phenotypes were later isolated: a female sterile allele results in a defect in a tissue-specific form of DNA synthesis (chorion gene amplification) and lethal alleles cause mitotic chromosome instability that can be observed genetically and cytologically [1].
• The Drosophila mus101 gene, which links DNA repair, replication and condensation of heterochromatin in mitosis, encodes a protein with seven BRCA1 C-terminus domains [1].
• We report here that mus101 encodes a member of the BRCT (BRCA1 C terminus) domain superfamily of proteins implicated in DNA repair and cell cycle checkpoint control [1].
• One mutant is an allele of a locus (mus-101) previously identified by mutagen-sensitive mutants and a second mutant is an allele of the lethal locus zw 10.--The 15 mutants were also examined cytologically for their effects on chromosomes in larval neuroblasts [3].

Other interactions of mus101

• In contrast, cells from five nonallelic postreplication repair-defective mutants (mei-41, mus101, mus205, mus302 and mus310) respond to ultraviolet light by synthesizing nascent DNA in abnormally short segments [4].
• The high dose part of the curve is sensitive to oxygenation during irradiation and is affected significantly by the mutants with low fertility (mei-9, mus101 and mus302) [5].
• Four female-sterile mutants, fs(1)K451, fs(1)K1214, fs(1)K575TS, and fs(1)384, were studied in terms of chorion structure and chorion protein composition [6].

References