The effects of 0 - 25 mM urethane, 0 - 50 muM selenocystine and 0 - 100 muM sodium monohydrogen arsenate on marker-exchange frequencies have been studied along a region of the X chromosome of Drosophila melanogaster marked by y, cv, v and f. Clear and consistent effects seen in concentration curves were usually but not always found significant in analyses of variance. Urethane concentration curves rose to a higher level at 0.5 to 3 mM and dropped to control levels between 10 and 25 mM. It is proposed that this reversibility was due to a competition between two categories of lesions mimicking natural recombination sites, those on unpaired regions of the chromosome competing with those on already paired regions for recombination-repair enzymes. Selenocystine affected exchange frequencies mainly toward the ends of the unmarked region, especially y - cv, negatively from 2 to 10 muM and positively above 10 muM. These effects are interpreted as being mediated by selenocystine control over restriction of synaptic pairing to terminal regions, especially y - cv. Interaction between urethane and selenocystine in two-chemical treatments satisfactorily support the above explantations for both the urethane and selenocystine effects. Sodium monohydrogen arsenate effects, tentatively attributed to the arsenate ion, differed markedly from those of the other chemicals: "arsenate" concentration curves for single-exchange classes tended to be broadly convex and those for double-exchange classes concave, while interactions with urethane tended to be synergistic or neutral except in one exchange class (that for single exchange in y - cv). No satisfactory explanation of the arsenate effects has yet been found. At 25 mM only, urethane caused male-specific, 95% pupal mortality.
[1]
P. Hastings.
A possible source of primary nucleotide chain breaks in recombinant structures in eukaryotes.
,
1972,
Genetical research.
[2]
A. Bell,et al.
The relative influence of sex of progeny on the lethal expression of the sonless gene in Drosophila melanogaster.
,
1972,
Genetics.
[3]
A. Bell,et al.
Sonless, a sex-ratio anomaly in Drosophila melanogaster resulting from a gene-cytoplasm interaction.
,
1970,
Genetics.
[4]
G. W. Walker,et al.
The distributive effect of selenoaminoacid treatment on crossing-over in Drosophila melanogaster.
,
1969,
Genetics.
[5]
Michio Ito,et al.
DNA-DEPENDENT FORMATION OF THE SYNAPTINEMAL COMPLEX AT MEIOTIC PROPHASE
,
1967,
The Journal of cell biology.
[6]
H. Taber,et al.
Inactivating DNA alterations induced by peroxides and peroxide-producing agents.
,
1967,
Mutation research.
[7]
S. Wolff,et al.
Chemistry of Crossing-over
,
1967,
Nature.
[8]
E. Boyland,et al.
The metabolism of urethane and related compounds
,
1965
.
[9]
R. E. Esposito,et al.
THE EFFECT OF 5-FLUORODEOXYURIDINE ON GENETIC REPLICATION AND MITOTIC CROSSING OVER IN SYNCHRONIZED CULTURES OF USTILAGO MAYDIS.
,
1964,
Genetics.
[10]
G. R. Mckinney.
The action of various drugs on certain phases of in vitro anabolism.
,
1950,
The Journal of pharmacology and experimental therapeutics.
[11]
H. H. Plough.
The effect of temperature on crossingover in Drosophila
,
1917
.