Investigations on the organization of genetic loci in Drosophila melanogaster: lethal mutations affecting 6-phosphogluconate dehydrogenase and their suppression

1977 ◽  
Vol 153 (2) ◽  
pp. 191-198 ◽  
Author(s):  
V. A. Gvozdev ◽  
T. I. Gerasimova ◽  
G. L. Kogan ◽  
J. M. Rosovsky
Genetics ◽  
1984 ◽  
Vol 106 (2) ◽  
pp. 249-265
Author(s):  
Jym Mohler ◽  
Mary Lou Pardue

ABSTRACT The region containing subdivisions 93C, 93D and 93E on chromosome 3 of Drosophila melanogaster has been screened for visible and lethal mutations. Treatment with three mutagens, γ irradiation, ethyl methanesulfonate and diepoxybutane, has produced mutations that fall into 20 complementation groups, including the previously identified ebony locus. No point mutations affecting the heat shock locus in 93D were detected; however, a pair of deficiencies that overlap in the region of this locus was isolated. Flies heterozygous in trans for this pair of deficiencies are capable of producing all of the major heat shock puffs (except 93D) and the major heat shock proteins. In addition, these flies show recovery of normal protein synthesis following a heat shock.


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.


Genetics ◽  
1982 ◽  
Vol 101 (3-4) ◽  
pp. 461-476
Author(s):  
Todd R Laverty ◽  
J K Lim

ABSTRACT In this study, we show that at least one lethal mutation at the 3F-4A region of the X chromosome can generate an array of chromosome rearrangements, all with one chromosome break in the 3F-4A region. The mutation at 3F-4A (secondary mutation) was detected in an X chromosome carrying a reverse mutation of an unstable lethal mutation, which was mapped in the 6F1-2 doublet (primary mutation). The primary lethal mutation at 6F1-2 had occurred in an unstable chromosome (Uc) described previously (Lim 1979). Prior to reversion, the 6F1-2 mutation had generated an array of chromosome rearrangements, all having one break in the 6F1-2 doublet (Lim 1979, 1980). In the X chromosomes carrying the 3F-4A secondary lethal mutation the 6F1-2 doublet was normal and stable, as was the 3F-4A region in the X chromosome carrying the primary lethal mutation. The disappearance of the instability having a set of genetic properties at one region (6F1-2) accompanied by its appearance elsewhere in the chromosome (3F-4A) implies that a transposition of the destabilizing element took place. The mutant at 3F-4A and other secondary mutants exhibited all but one (reinversion of an inversion to the normal sequence) of the eight properties of the primary lethal mutations. These observations support the view that a transposable destabilizing element is responsible for the hypermutability observed in the unstable chromosome and its derivaties.


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 ◽  
1985 ◽  
Vol 87 (1) ◽  
pp. 99-114
Author(s):  
Alfonso Martinez-Arias

The mutant fused (1–59·5) belongs to a class of lethal mutations in Drosophila melanogaster that produce pattern duplications in every segment of the mature embryo. A study of the embryonic development of fused'− embryos derived horn fused− mothers shows that extensive cell death occurs early in development. This cell death accounts for the smaller size of the segments in fused− embryos. The pattern duplication observed is, probably, a secondary consequence of the pattern deletion.


Genome ◽  
1989 ◽  
Vol 32 (1) ◽  
pp. 146-154 ◽  
Author(s):  
G. N. Goulielmos ◽  
S. N. Alahiotis

In spite of previous consensus that no F1 fertile hybrids (of both sexes) could be produced between any mating combination of Drosophila melanogaster, D. simulans, and D. mauritiana, the present data indicate that such hybrids were obtained. Thus, some crosses between D. mauritiana females and D. simulans or D. melanogaster males yield F1 fertile hybrids (of both sexes) which have been named Masi (or Masi-2 and Masi-3) and Mame, respectively. Electrophoretic studies, using the species-diagnostic genes for 6-phosphogluconate dehydrogenase, alcohol dehydrogenase, and aldehyde oxidase (6-Pgd, Adh, and Aldox, respectively), were used to investigate the hybrid status, taking into consideration (i) their reproductive relationships, (ii) the coexistence of electromorphs from different species in the same hybrid, within the same generation, and (iii) the expression of the above electromorphs in the hybrids as well as in progeny from backcrosses, where unexpected irregularities and abnormalities were observed. These interspecific hybrids have been kept in our laboratory (as stocks) for 50 generations, to date, and have also been tested for various characteristics that contributed to the verification of their hybrid status (mating abilities, enzyme activities, hybrid sex ratio, the morphology of male genital arches and other fitness components). The finding of major genetic phenomena (e.g., allozymic repression) in these hybrid genomes gives some idea of the nature of events that could be associated with strong evolutionary changes, thus controlling speciation processes.Key words: Drosophila, electrophoresis, electromorphs, interspecific hybrids.


Genetics ◽  
1983 ◽  
Vol 105 (2) ◽  
pp. 371-386
Author(s):  
Michael A Kotarski ◽  
Sally Pickert ◽  
Ross J MacIntyre

ABSTRACT The chromosomal region surrounding the structural gene for α-glycerophosphate dehydrogenase (αGpdh, 2-20.5) of Drosophila melanogaster has been studied in detail. Forty-three EMS-induced recessive lethal mutations and five previously identified visible mutations have been localized within the 25A-27D region of chromosome 2 by deficiency mapping and in some cases by a recombination analysis. The 43 lethal mutations specify 17 lethal loci. ?Gpdh has been localized to a single polytene chromosome band, 25F5, and there apparently are no lethals that map to the αGpdh locus.


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