scholarly journals PERSISTENCE OF RECESSIVE LETHAL GENES ON THE SECOND CHROMOSOME OF DROSOPHILA MELANOGASTER IN EXPERIMENTAL POPULATIONS

1971 ◽  
Vol 46 (3) ◽  
pp. 159-167
Author(s):  
SHIGEMITSU TANO
Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut

ABSTRACT When females of Drosophila melanogaster are treated with chemical or physical mutagens, not only in one but also in both of the two homologous X chromosomes of a given oocyte, a recessive sex-linked lethal mutation may be induced. A method is described that discriminates between such "single" and "double mutations." A theory is developed to show how a comparison between the expected and the observed frequency of double mutations yields an indication of the intercellular distribution (random or nonrandom) of recessive lethal mutations induced by mutagenic agents in oocytes and, consequently, of the distribution (homogeneous or nonhomogeneous) of those agents.—Three agents were tested: FUdR (12.5, 50.0 and 81.0,μg/ml), mitomycin C (130.0 μg/ml) and X rays (2000 R, 150 kV). After FUdR feeding, no increase in the mutation frequency usually observed in D. melanogaster without mutagenic treatment was obtained (u=0.13%, namely three single mutations among 2332 chromosomes tested). After mitomycin C feeding, 104. single and three double mutations were obtained. All of the 50 mutations observed after X irradiation were single mutations. The results obtained in the mitomycin C and radiation experiments favor the assumption of a random intercellular distribution of recessive lethal mutations induced by these two agents in oocytes of D. melanogaster. Reasons are discussed why for other types of mutagenic agents nonrandom distributions may be observed with our technique.


1974 ◽  
Vol 24 (1) ◽  
pp. 1-10 ◽  
Author(s):  
J. K. Lim ◽  
L. A. Snyder

SUMMARYSalivary-gland chromosomes of 54 methyl methanesulphonate- and 50 triethylene melamine-induced X-chromosome recessive lethals in Drosophila melanogaster were analysed. Two of the lethals induced by the mono-functional agent and 11 of those induced by the polyfunctional agent were found to be associated with detectable aberrations. A complementation analysis was also done on 82 ethyl methanesulphonate- and 34 triethylene melamine-induced recessive lethals in the zeste-white region of the X chromosome. The EMS-induced lethals were found to represent lesions affecting only single cistrons. Each of the 14 cistrons in the region known to mutate to a lethal state was represented by mutant alleles, but in widely different frequencies. Seven of the TEM-induced lethals were associated with deletions, only one of which had both breakpoints within the mapped region. Twenty-six of the 27 mutations in which only single cistrons were affected were mapped to 7 of the 14 known loci. One TEM- and two EMS-induced mutations were alleles representing a previously undetected locus in the zeste-white region.


Development ◽  
1966 ◽  
Vol 16 (3) ◽  
pp. 559-568
Author(s):  
Louie Hamilton

The problem of the factors involved in the development of the haploid syndrome in anuran embryos is as yet unsolved. It is known that about 90 % of all haploid frog embryos develop the haploid syndrome, which is characterized by the presence of oedema and sluggishness, by reduction in pigmentation and in the efficiency of the heart and circulation, and by a partial failure of the gut to coil and of muscle to differentiate. The two most favoured explanations of the development of the haploid syndrome have been nucleocytoplasmic imbalance, since a haploid nucleus is only half the size of a diploid nucleus in the same-sized egg, and unmasked recessive lethal genes. There is good evidence that an abnormal nucleocytoplasmic ratio is an important contributory factor in the development of the haploid syndrome. Briggs (1949) compared populations of haploids developing from large and small eggs and Subtelny (1958) compared the development of haploids and homozygous diploids which possessed a reduplicated set of haploid chromosomes.


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