THE HYPERMUTABILITY CONFERRED BY THE MUS308 MUTATION OF DROSOPHILA IS NOT SPECIFIC FOR CROSS-LINKING AGENTS

被引：19

作者：

AGUIRREZABALAGA, I ^{[1
]}

SIERRA, LM ^{[1
]}

COMENDADOR, MA ^{[1
]}

机构：

[1] UNIV OVIEDO,DEPT BIOL FUNC,AREA GENET,E-33071 OVIEDO,SPAIN

来源：

MUTATION RESEARCH-DNA REPAIR | 1995年 / 336卷 / 03期

关键词：

DROSOPHILA MELANOGASTER; MUS308; HYPERMUTABILITY; DNA CROSS-LINKS; POSTREPLICATION REPAIR;

D O I：

10.1016/0921-8777(94)00057-D

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

The hypersensitivity of the mus308 mutant of D. melanogaster to cross-linking agents has been suggested to be the consequence of a possible defect of this mutant in DNA cross-link repair. Moreover, the mus308 mutation has been proposed as an animal model for the study of Fanconi's anemia. In order to obtain more information about the function controlled by this locus, we have measured the mutability of the mus308 mutant to several mutagens with different modes of action using the sex-linked recessive lethal test. We show that this mutation confers hypermutability not only to the cross-linking agents tested, hexamethylphosphoramide and hexamethylmelamine, but to the point mutagen N-ethyl-N-nitrosourea as well, whereas the response to methyl methanesulfonate was normal. The results suggest that the mus308 locus is not defective in a repair pathway specific for cross-links but is rather involved in a step of a more general post-replication repair process responsible for the removal of non-excised adducts.

引用

页码：243 / 250

页数：8

共 38 条

[11] REPAIR OF O-ALKYLPYRIMIDINES IN MAMMALIAN-CELLS - A PRESENT CONSENSUS [J].

BRENT, TP ;

DOLAN, ME ;

FRAENKELCONRAT, H ;

HALL, J ;

KARRAN, P ;

LAVAL, F ;

MARGISON, GP ;

MONTESANO, R ;

PEGG, AE ;

POTTER, PM ;

SINGER, B ;

SWENBERG, JA ;

YAROSH, DB .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (06) :1759-1762

[12] ABNORMAL RECOVERY OF DNA-REPLICATION IN ULTRAVIOLET-IRRADIATED CELL-CULTURES OF DROSOPHILA-MELANOGASTER WHICH ARE DEFECTIVE IN DNA-REPAIR [J].

BROWN, TC ;

BOYD, JB .

MOLECULAR & GENERAL GENETICS, 1981, 183 (02) :363-368

[13] STUDIES ON MUTAGEN-SENSITIVE STRAINS OF DROSOPHILA-MELANOGASTER .9. MODIFICATION OF GENETIC-DAMAGE INDUCED BY X-IRRADIATION OF SPERMATOZOA IN N-2, AIR OR O-2 BY 4 AUTOSOMAL REPAIR-DEFICIENT MUTANTS [J].

FERRO, W .

MUTATION RESEARCH, 1986, 166 (01) :49-57

[14]

FINKELBERG R, 1977, AM J HUM GENET, V29, pA42

[15]

GATTI M, 1984, GENETICS NEW FRONTIE, P193

[16] MUTAGENIC PROCESSING OF PSORALEN MONOADDUCTS DIFFER IN NORMAL AND FANCONI-ANEMIA CELLS [J].

GUILLOUF, C ;

LAQUERBE, A ;

MOUSTACCHI, E ;

PAPADOPOULO, D .

MUTAGENESIS, 1993, 8 (04) :355-361

[17] A DAMAGE-RECOGNITION PROTEIN WHICH BINDS TO DNA CONTAINING INTERSTRAND CROSS-LINKS IS ABSENT OR DEFECTIVE IN FANCONI-ANEMIA, COMPLEMENTATION GROUP-A, CELLS [J].

HANG, B ;

YEUNG, AT ;

LAMBERT, MW .

NUCLEIC ACIDS RESEARCH, 1993, 21 (18) :4187-4192

[18] REEVALUATION OF EXCISION REPAIR IN THE MUS304, MUS306 AND MUS308 MUTANTS OF DROSOPHILA [J].

HARRIS, PV ;

BOYD, JB .

MUTATION RESEARCH, 1993, 301 (01) :51-55

[19]

ISHIDA R, 1982, CANCER RES, V42, P4000

[20] DEFECTIVE-DNA ENDONUCLEASE ACTIVITIES IN FANCONIS ANEMIA CELLS, COMPLEMENTATION GROUP-A AND GROUP-B [J].

LAMBERT, MW ;

TSONGALIS, GJ ;

LAMBERT, WC ;

HANG, B ;

PARRISH, DD .

MUTATION RESEARCH, 1992, 273 (01) :57-71

← 1 2 3 4 →