TY - JOUR
T1 - The mus206 gene of Drosophila melanogaster is required in the excision repair of alkylation-induced DNA lesions
AU - Huang, Wenya
AU - Smith, P. Dennis
N1 - Funding Information:
The authors are pleased to acknowledge the contributions of Dr. Ruth L. Dusenbery and the technical assistance of Thomas Shehab and Susan Uptain. Support for this project was provided by the Office of the Vice President for Research, the College of Science and the Department of Biological Sciences of Wayne State University. Kathy Matthews of the Drosophila Stock Center at Indiana University, Bloomington and Phyllis Oster of the Drosophila Stock Center at Bowling Green State University have provided continued resource support for the Principal Investigator's laboratory and we are pleased to recognize their valuable assistance.
PY - 1997/8
Y1 - 1997/8
N2 - The mus206(A1) mutation, previously identified in our laboratory on the basis of increased sensitivity to methyl methanesulfonate (MMS), has undergone further analysis. Genetic recombinational mapping data localize mus206 at 2-54.8. Sex-linked recessive lethal mutation tests indicate that mus206(A1) exhibits significant alkylation-induced hypermutability, compared to the wild-type Oregon R progenitor strain, suggesting a defect in DNA repair function. Results of embryo viability tests show that mus206(A1) and Oregon R embryos hatch to the first instar larvae at similar rates, indicating that the mus206(A1) mutation does not confer embryonic lethality. Unscheduled DNA synthesis (UDS) studies with primary embryonic cell cultures subsequently demonstrated considerably less nucleotide incorporation following treatment with MMS, confirming that mus206(A1) is deficient at or before the resynthesis step of alkylation-induced DNA excision repair. Previous genetic investigations have provided indirect support that at least 15 Drosophila genes which display MMS sensitivity are deficient in DNA repair functions. This study brings to 7 the number of mus genes displaying alkylation excision-repair deficiency.
AB - The mus206(A1) mutation, previously identified in our laboratory on the basis of increased sensitivity to methyl methanesulfonate (MMS), has undergone further analysis. Genetic recombinational mapping data localize mus206 at 2-54.8. Sex-linked recessive lethal mutation tests indicate that mus206(A1) exhibits significant alkylation-induced hypermutability, compared to the wild-type Oregon R progenitor strain, suggesting a defect in DNA repair function. Results of embryo viability tests show that mus206(A1) and Oregon R embryos hatch to the first instar larvae at similar rates, indicating that the mus206(A1) mutation does not confer embryonic lethality. Unscheduled DNA synthesis (UDS) studies with primary embryonic cell cultures subsequently demonstrated considerably less nucleotide incorporation following treatment with MMS, confirming that mus206(A1) is deficient at or before the resynthesis step of alkylation-induced DNA excision repair. Previous genetic investigations have provided indirect support that at least 15 Drosophila genes which display MMS sensitivity are deficient in DNA repair functions. This study brings to 7 the number of mus genes displaying alkylation excision-repair deficiency.
UR - https://www.scopus.com/pages/publications/0030837957
UR - https://www.scopus.com/pages/publications/0030837957#tab=citedBy
U2 - 10.1016/S0921-8777(97)00015-3
DO - 10.1016/S0921-8777(97)00015-3
M3 - Review article
C2 - 9298117
AN - SCOPUS:0030837957
SN - 0921-8777
VL - 384
SP - 81
EP - 88
JO - Mutation Research - DNA Repair
JF - Mutation Research - DNA Repair
IS - 2
ER -