Genetical and Cytological Studies of Lethals induced by Chemical Treatment in Drosophila melanogaster.

1945 ◽  
Vol 62 (3) ◽  
pp. 234-242 ◽  
Author(s):  
Helen Slizynska ◽  
B. M. Slizynski
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Chemical Treatment ◽  
Structural Changes ◽  
Chromosomal Rearrangements ◽  
Point Mutations ◽  
Ultra Violet ◽  
Lethal Effect ◽  
Structural Elements ◽  
Adult Males

The present paper forms a continuation of studies of recessive sex-linked lethals in Drosophila melanogaster published previously (1938, 1941). In these, lethals occurring spontaneously, induced by X-ray treatment and by ultra-violet light were examined cytologically in the salivary gland chromosomes.The genetic factors which stop or change the development of an individual in such a way that its death ensues under normal conditions are termed lethals. A lethal effect may be connected with a mutation of a gene or with its absence from the chromosome: those which cannot be proved to be associated with the absence of a cytologically detectable part of the chromosome are considered as due to “point” mutations.The absence of a microscopically identifiable section of a chromosome with all its genetical and structural elements is called a deficiency. With few exceptions (Muller, 1935; Demerec and Hoover, 1936) the deficiencies in the X-chromosome, whatever their size and whatever loci they involve, are lethal for males. In females heterozygous for them deficiencies of small or even moderate size usually do not produce any visible phenotypical effect, although some cases are known (Mohr, 1923; Slizynska, 1938) in which a heterozygous deficiency for a particular band is always associated with a definite phenotype. Thus a lethal effect may or may not be the result of a deficiency, while a deficiency in the X-chromosome almost always has a lethal effect in the males.In 1941 Auerbach (1943, 1946 in press) succeeded in producing “visible” and lethal mutations and chromosomal rearrangements by chemical treatment in which adult males were exposed to vapours of (C1CH2CH2)2S in a specially designed apparatus. The object of this paper is to show what proportion of sex-linked recessive lethals produced in Drosophila melanogaster by these new agents is connected with detectable deficiencies. Besides finding out whether chemically produced lethals are associated with detectable deficiencies, the problem of the relation between lethals and “visible” mutations is discussed on the basis of their respective distributions along the chromosome. It should be stated that the lethals connected with gross structural changes represent probably only a small fraction of such lethals actually produced since many of them were eliminated by zygotic lethality.

scholarly journals Examination of a mutable system affecting the components of the segregation distorter meiotic drive system of Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 125 (1) ◽  
pp. 51-76
Author(s):  
K G Golic
Keyword(s):  
Drosophila Melanogaster ◽  
Transposable Element ◽  
X Chromosome ◽  
Segregation Distortion ◽  
Chromosomal Rearrangements ◽  
Meiotic Drive ◽  
Drive System ◽  
Partial Loss ◽  
Segregation Distorter ◽  
Relationship Of

Abstract Segregation distortion in Drosophila melanogaster is the result of an interaction between the genetic elements Sd, a Rsp sensitive to Sd, and an array of modifiers, that results in the death of sperm carrying Rsp. A stock (designated M-5; cn bw) has been constructed which has the property of inducing the partial loss of sensitivity from previously sensitive cn bw chromosomes, the partial loss of distorting ability from SD chromosomes, and a concomitant acquisition of modifiers on the X chromosome and possibly also on the autosomes. By several criteria the changes exhibited under the influence of M-5; cn bw are characteristic of the transposable-element systems which produce hybrid dysgenesis. In the first place, the magnitude of these effects depends on the nature of the crosses performed. The analogy is further strengthened by the observation that the changes induced by M-5; cn bw share other stigmata of Drosophila transposable-element systems, including high sterility among the progeny of outcrosses, and the production of chromosomal rearrangements. The possible relationship of this system to the P, I and hobo transposable element systems is discussed, as well as its bearing on aspects of the Segregation Distorter phenomenon which have yet to be explained.

scholarly journals The Haplolethal Region at the 16F Gene Cluster of Drosophila melanogaster: Structure and Function

Genetics ◽  
1999 ◽  
Vol 151 (1) ◽  
pp. 163-175 ◽  
Author(s):  
Antonio Prado ◽  
Inmaculada Canal ◽  
Alberto Ferrús
Keyword(s):  
Drosophila Melanogaster ◽  
Troponin I ◽  
Muscle Protein ◽  
Chromosomal Rearrangements ◽  
Regulatory Region ◽  
Lethal Effect ◽  
Functional Expression ◽  
Transcription Unit ◽  
Dominant Lethal ◽  
And Function

Abstract Extensive aneuploid analyses had shown the existence of a few haplolethal (HL) regions and one triplolethal region in the genome of Drosophila melanogaster. Since then, only two haplolethals, 22F1-2 and 16F, have been directly linked to identified genes, dpp and wupA, respectively. However, with the possible exception of dpp, the actual bases for this dosage sensitivity remain unknown. We have generated and characterized dominant-lethal mutations and chromosomal rearrangements in 16F and studied them in relation to the genes in the region. This region extends along 100 kb and includes at least 14 genes. The normal HL function depends on the integrity of a critical 4-kb window of mostly noncoding sequences within the wupA transcription unit that encodes the muscle protein troponin I (TNI). All dominant lethals are breakpoints within that window, which prevent the functional expression of TNI and other adjacent genes in the proximal direction. However, independent mutations in these genes result in recessive lethal phenotypes only. We propose that the HL at 16F represents a long-range cis regulatory region that acts upon a number of functionally related genes whose combined haploidy would yield the dominant-lethal effect.

A novel genetic interaction between daughterless and a variegating rearrangement strain of Drosophila melanogaster

Genome ◽  
1995 ◽  
Vol 38 (1) ◽  
pp. 105-111
Author(s):  
Dalia Chakrabarti ◽  
Somnath Mukhopadhyay ◽  
Ashish K. Duttagupta
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Maternal Effect ◽  
Genetic Interaction ◽  
Position Effect ◽  
Lethal Effect

The effect of the maternal-effect mutation daughterless (da) on the reinverted In(1)BM2 strain of Drosophila melanogaster has been evaluated cytogenetically. Results show that while the variegated nature of the single X chromosome of In(1)BM2(rv) males born to ♂ da/da × ♀ +/+ parents is suppressed, their female sibs, homozygous for the In(1)BM2(rv) chromosome, survive the lethal effect of the absence of da+ product in their zygotes.Key words: Drosophila, variegation, modifier of variegation, position effect.

scholarly journals MUTATIONAL ANALYSIS OF THE REGION SURROUNDING THE 93D HEAT SHOCK LOCUS OF DROSOPHILA MELANOGASTER

Genetics ◽  
1984 ◽  
Vol 106 (2) ◽  
pp. 249-265
Author(s):  
Jym Mohler ◽  
Mary Lou Pardue
Keyword(s):  
Drosophila Melanogaster ◽  
Heat Shock ◽  
Mutational Analysis ◽  
Point Mutations ◽  
Γ Irradiation ◽  
Lethal Mutations ◽  
Complementation Groups ◽  
In Trans ◽  
Shock Locus ◽  
Shock Proteins

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.

scholarly journals Patterns of DNA Variability at X-Linked Loci in Mus domesticus

Genetics ◽  
1997 ◽  
Vol 147 (3) ◽  
pp. 1303-1316
Author(s):  
Michael W Nachman
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
House Mouse ◽  
Recombination Rate ◽  
Nucleotide Diversity ◽  
Mus Domesticus ◽  
Substantial Variation ◽  
Intraspecific Polymorphism ◽  
Recombination Rates ◽  
Interspecific Divergence

Introns of four X-linked genes (Hprt, Plp, Glra2, and Amg) were sequenced to provide an estimate of nucleotide diversity at nuclear genes within the house mouse and to test the neutral prediction that the ratio of intraspecific polymorphism to interspecific divergence is the same for different loci. Hprt and Plp lie in a region of the X chromosome that experiences relatively low recombination rates, while Glra2 and Amg lie near the telomere of the X chromosome, a region that experiences higher recombination rates. A total of 6022 bases were sequenced in each of 10 Mus domesticus and one M. caroli. Average nucleotide diversity (π) for introns within M. domesticus was quite low (π = 0.078%). However, there was substantial variation in the level of heterozygosity among loci. The two telomeric loci, Glra2 and Amg, had higher ratios of polymorphism to divergence than the two loci experiencing lower recombination rates. These results are consistent with the hypothesis that heterozygosity is reduced in regions with lower rates of recombination, although sampling of additional genes is needed to establish whether there is a general correlation between heterozygosity and recombination rate as in Drosophila melanogaster.

scholarly journals SITE-SPECIFIC INSTABILITY IN DROSOPHILA MELANOGASTER: EVIDENCE FOR TRANSPOSITION OF DESTABILIZING ELEMENT

Genetics ◽  
1982 ◽  
Vol 101 (3-4) ◽  
pp. 461-476
Author(s):  
Todd R Laverty ◽  
J K Lim
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Lethal Mutation ◽  
Chromosome Rearrangements ◽  
Chromosome Break ◽  
Secondary Mutation ◽  
X Chromosomes ◽  
Site Specific ◽  
Normal Sequence ◽  
Lethal Mutations

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.

scholarly journals Hybrid dysgenesis-induced quantitative variation on the X chromosome of Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 627-636
Author(s):  
C Q Lai ◽  
T F Mackay
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Quantitative Traits ◽  
Natural Populations ◽  
Quantitative Variation ◽  
Hybrid Dysgenesis ◽  
X Chromosomes ◽  
Bristle Number ◽  
Seven Generations ◽  
Polygenic Variation

Abstract To determine the ability of the P-M hybrid dysgenesis system of Drosophila melanogaster to generate mutations affecting quantitative traits, X chromosome lines were constructed in which replicates of isogenic M and P strain X chromosomes were exposed to a dysgenic cross, a nondysgenic cross, or a control cross, and recovered in common autosomal backgrounds. Mutational heritabilities of abdominal and sternopleural bristle score were in general exceptionally high-of the same magnitude as heritabilities of these traits in natural populations. P strain chromosomes were eight times more mutable than M strain chromosomes, and dysgenic crosses three times more effective than nondysgenic crosses in inducing polygenic variation. However, mutational heritabilities of the bristle traits were appreciable for P strain chromosomes passed through one nondysgenic cross, and for M strain chromosomes backcrossed for seven generations to inbred P strain females, a result consistent with previous observations on mutations affecting quantitative traits arising from nondysgenic crosses. The new variation resulting from one generation of mutagenesis was caused by a few lines with large effects on bristle score, and all mutations reduced bristle number.

Specificity of Chromosome Damage Caused by the Rex Element of Drosophila melanogaster

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 109-115 ◽  
Author(s):  
Leonard G Robbins
Keyword(s):  
Drosophila Melanogaster ◽  
Early Development ◽  
X Chromosome ◽  
Ribosomal Rna ◽  
Chromosome Damage ◽  
Genetic Element ◽  
Single Chromosome ◽  
Experimental Cross ◽  
Rdna Array ◽  
Early Embryos

Abstract Rex is a multicopy genetic element that maps within an X-linked ribosomal RNA gene (rDNA) array of D. melanogaster. Acting maternally, Rex causes recombination between rDNA arrays in a few percent of early embryos. With target chromosomes that contain two rDNA arrays, the exchanges either delete all of the material between the two arrays or invert the entire intervening chromosomal segment. About a third of the embryos produced by Rex homozygotes have cytologically visible chromosome damage, nearly always involving a single chromosome. Most of these embryos die during early development, displaying a characteristic apoptosis-like phenotype. An experiment that tests whether the cytologically visible damage is rDNA-specific is reported here. In this experiment, females heterozygous for Rex and an rDNA-deficient X chromosome were crossed to males of two genotypes. Some of the progeny from the experimental cross entirely lacked rDNA, while all of the progeny from the control cross had at least one rDNA array. A significantly lower frequency of early-lethal embryos in the experimental cross, proportionate to the fraction of rDNA-deficient embryos, demonstrates that Rex preferentially damages rDNA.

scholarly journals Cytogenetic and complementation analyses of recessive lethal mutations induced in the X chromosome of Drosophila by three alkylating agents

1974 ◽  
Vol 24 (1) ◽  
pp. 1-10 ◽  
Author(s):  
J. K. Lim ◽  
L. A. Snyder
Keyword(s):  
Drosophila Melanogaster ◽  
Salivary Gland ◽  
X Chromosome ◽  
Alkylating Agents ◽  
Complementation Analysis ◽  
Ethyl Methanesulphonate ◽  
Induced Mutations ◽  
Recessive Lethal ◽  
Lethal Mutations

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.

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