P32-INDUCED LETHAL MUTATIONS IN DROSOPHILA

1951 ◽  
Vol 29 (3) ◽  
pp. 234-239 ◽  
Author(s):  
T. J. Arnason ◽  
R. L. Irwin ◽  
J. W. T. Spinks
Keyword(s):  
X Rays ◽  
Total Radiation ◽  
Wild Type ◽  
Larval Food ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Initial Concentration ◽  
Lethal Mutations ◽  
Total Radiation Dose ◽  
Food Medium

X-chromosomes of P32-treated wild-type Drosophila melanogaster were tested for the presence of recessive lethal mutations. Treated larvae were reared in food medium containing initially 6.5, 32.5, 65.0, or 162.5 mrd. P32 per ml. Of 838 tested chromosomes 42 had recessive lethals. The frequency of mutation was roughly proportional to P32 content of the food. An initial concentration of 18.8 mrd. P32 in larval food is expected to produce about the same frequency of recessive lethal mutations as is obtained with 1000 r. of X rays applied to mature sperm. A fly reared in medium having an initial concentration of 32.5 mrd. per ml. receives, prior to mating, a calculated total radiation dose of 0.62 gram roentgens. At this dosage 4.2% recessive lethals were recorded. For equivalent amounts of ionization P32 is here apparently 2.3 times as effective as X rays.

scholarly journals THE INTERCELLULAR DISTRIBUTION OF MUTATIONS INDUCED IN OOCYTES OF DROSOPHILA MELANOGASTER BY CHEMICAL AND PHYSICAL MUTAGENS

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut
Keyword(s):  
Drosophila Melanogaster ◽  
Mitomycin C ◽  
Mutation Frequency ◽  
Lethal Mutation ◽  
X Rays ◽  
Mutagenic Treatment ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
X Irradiation

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.

scholarly journals MALE-STERILIZING INTERACTIONS BETWEEN DUPLICATIONS AND DEFICIENCIES FOR PROXIMAL X-CHROMOSOME MATERIAL IN DROSOPHILA MELANOGASTER

Genetics ◽  
1981 ◽  
Vol 99 (1) ◽  
pp. 49-64
Author(s):  
Rezaur Rahman ◽  
Dan L Lindsley
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Male Fertility ◽  
Primary Spermatocyte ◽  
Single Factor ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Y Chromosomes ◽  
Chromosome Material

ABSTRACT The genetic limits of sixty-four deficiencies in the vicinity of the euchromatic-heterochromatic junction of the X chromosome were mapped with respect to a number of proximal recessive lethal mutations. They were also tested for male fertility in combination with three Y chromosomes carrying different amounts of proximal X-chromosome-derived material (BSYy+, y+Ymal126 and y  +  Ymal  +). All deficiencies that did not include the locus of bb and a few that did were male-fertile in all male-viable Df(1)/Dp(1;Y) combinations. Nineteen bb deficiencies fell into six different classes by virtue of their male-fertility phenotypes when combined with the duplicated Y chromosomes. The six categories of deficiencies are consistent with a formalism that invokes three factors or regions at the base of the X, one distal and two proximal to bb, which bind a substance critical for precocious inactivation of the X chromosome in the primary spermatocyte. Free duplications carrying these regions or factors compete for the substance in such a way that, in the presence of such duplications, proximally deficient X chromosomes are unable to command sufficient substance for proper control of X-chromosome gene activity preparatory to spermatogenesis. We conclude that there is no single factor at the base of the X that is required for the fertility of males whose genotype is otherwise normal.

THE NONMUTAGENIC ACTION OF p-p′-DDT AND γ-HEXACHLOROCYCLOHEXANE IN DROSOPHILA MELANOGASTER MEIG. (DIPTERA: DROSOPHILIDAE)

1952 ◽  
Vol 30 (6) ◽  
pp. 375-377 ◽  
Author(s):  
D. P. Pielou
Keyword(s):  
Drosophila Melanogaster ◽  
Selective Breeding ◽  
Larval Feeding ◽  
Mutagenic Action ◽  
Wild Type ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Insecticide Tolerance ◽  
Feeding Medium ◽  
Insect Parasites

As experiments are in progress on selective breeding for insecticide tolerance in insect parasites and as various physiologically potent chemicals have been shown to cause mutation in Drosophila melanogaster Meig., tests were made to determine whether p-p′-DDT and γ-hexachlorocyclohexane had any mutagenic action. Wild type males of D. melanogaster that had been exposed to the former insecticide in their larval feeding medium, or, as adults, to the vapor of the latter insecticide, were tested. The Muller-5 method of detecting recessive lethal mutations in the X chromosome was used. No evidence of mutagenic action was found in either insecticidal isomer.

scholarly journals CHROMOSOME REARRANGEMENTS IN CAENORHABDITIS ELEGANS

Genetics ◽  
1976 ◽  
Vol 83 (1) ◽  
pp. 91-105
Author(s):  
Robert K Herman ◽  
Donna G Albertson ◽  
Sydney Brenner
Keyword(s):  
Linkage Group ◽  
Fluorescence Microscopy ◽  
The Other ◽  
Crossing Over ◽  
Group V ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
C Elegans ◽  
Lethal Mutations ◽  
Chromosome Fragments

ABSTRACT A method for selecting unlinked duplications of a part of the X chromosome of C. elegans is described. Five such duplications have been identified. One of them, Dp(X;V)1, is translocated to linkage group V, where it suppresses crossing over along the left half of linkage group V. Dp(X;V)1 homozygotes grow slowly and are sterile. The other four duplications are associated with chromosome fragments, as observed cytologically by fluorescence microscopy, and tend to be lost. Their frequency of loss is higher in strains homozygous for a mutation that promotes nondisjunction of X chromosomes. The recombination frequencies between two of these duplications and the X have been measured: the frequencies are at least 50 times less than for X-X recombination in the same region. The duplications may prove useful as balancers of recessive lethal mutations.

SOME EFFECTS OF P32 ON THE DEVELOPMENT OF DROSOPHILA

1949 ◽  
Vol 27d (4) ◽  
pp. 186-194 ◽  
Author(s):  
T. J. Arnason ◽  
R. L. Irwin ◽  
J. W. T. Spinks
Keyword(s):  
Culture Media ◽  
Larval Period ◽  
X Chromosomes ◽  
Calculated Concentration ◽  
Recessive Lethal ◽  
Initial Concentration ◽  
Lethal Genes

When freshly laid Drosophila eggs were placed in a graded series of P32 concentrations in the culture media, death of treated individuals occurred most frequently at the end of the larval period and in the pupal stages. No adults emerged from cultures having an initial concentration of 0.65 rutherford (rd.) or higher per ml. food. The calculated concentration of P32 expected to reduce emergence of adults to 50% is 0.120 rd. per ml. A dosage of 1.30 rd. per ml. prevents transformation of larvae to pupae. Three out of 132 X-chromosomes from males reared in medium having an initial concentration of 0.0325 rd. per ml. carried new recessive lethal "genes".

scholarly journals An attempt to estimate the induction by X-rays of recessive lethal and visible mutations in mice

1961 ◽  
Vol 2 (2) ◽  
pp. 296-305 ◽  
Author(s):  
T. C. Carter ◽  
Mary F. Lyon
Keyword(s):  
Mutation Rates ◽  
Corpora Lutea ◽  
X Rays ◽  
Male Mice ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
A Value ◽  
Specific Locus ◽  
Size At Birth ◽  
Lethal Genes

The experiment was designed to form a bridge between the results of specific-locus experiments, using only a few gene loci, and those using the whole genome of the mouse. Male mice were given 600 r acute X-rays and bred from in such a way that at successive stages mutation in spermatogonia to dominant visibles and lethals, dominant semisteriles, recessive visibles and recessive lethals could be measured. The data concerning dominant mutations were relatively few but confirmed previous results. No recessive visible mutations were found, and the upper fiducial limit to the induced mutation rate to recessive visibles was set at a value 4500 times the rate to viable specific-locus mutations. From the attempt to measure recessive lethal mutations two interesting points emerged. The first was that granddaughters of the irradiated males had fewer corpora lutea per pregnancy than granddaughters of the control males, and the second was that this difference in number of ova shed was not reflected in any difference in litter-size at birth. Since this suggests intra-uterine compensation, no attempt was made to calculate mutation rates to recessive lethal genes from these data. The implications of the results are discussed.

scholarly journals The let-60 locus controls the switch between vulval and nonvulval cell fates in Caenorhabditis elegans.

Genetics ◽  
1990 ◽  
Vol 126 (4) ◽  
pp. 899-913 ◽  
Author(s):  
M Han ◽  
R V Aroian ◽  
P W Sternberg
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Interaction ◽  
Dominant Negative ◽  
Loss Of Function ◽  
Wild Type ◽  
Gain Of Function ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Anchor Cell ◽  
Inductive Signal

Abstract During induction of the Caenorhabditis elegans hermaphrodite vulva by the anchor cell of the gonad, six multipotent vulval precursor cells (VPCs) have two distinct fates: three VPCs generate the vulva and the other three VPCs generate nonspecialized hypodermis. Genes that control the fates of the VPCs in response to the anchor cell signal are defined by mutations that cause all six VPCs to generate vulval tissue (Multivulva or Muv) or that cause all six VPCs to generate hypodermis (Vulvaless or Vul). Seven dominant Vul mutations were isolated as dominant suppressors of a lin-15 Muv mutation. These mutations are dominant alleles of the gene let-60, previously identified only by recessive lethal mutations. Our genetic studies of these dominant Vul recessive lethal mutations, recessive lethal mutations, intragenic revertants of the dominant Vul mutations, and the closely mapping semi-dominant multivulva lin-34 mutations suggest that: (1) loss-of-function mutations of let-60 are recessive lethal at a larval stage, but they also cause a Vul phenotype if the lethality is rescued maternally by a lin-34 gain-of-function mutation. (2) The dominant Vul alleles of let-60 are dominant negative mutations whose gene products compete with wild-type activity. (3) lin-34 semidominant Muv alleles are either gain-of-function mutations of let-60 or gain-of-function mutations of an intimately related gene that elevates let-60 activity. We propose that let-60 activity controls VPC fates. In a wild-type animal, reception by a VPC of inductive signal activates let-60, and it generates into a vulval cell type; in absence of inductive signal, let-60 activity is low and the VPC generates hypodermal cells. Our genetic interaction studies suggest that let-60 acts downstream of let-23 and lin-15 and upstream of lin-1 and lin-12 in the genetic pathway specifying the switch between vulval and nonvulval cell types.

scholarly journals UNEQUAL CROSSING OVER AT THE rRNA TANDON AS A SOURCE OF QUANTITATIVE GENETIC VARIATION IN DROSOPHILA

Genetics ◽  
1980 ◽  
Vol 95 (3) ◽  
pp. 727-742 ◽  
Author(s):  
R Frankham ◽  
D A Briscoe ◽  
R K Nurthen
Keyword(s):  
Genetic Variation ◽  
Selection Response ◽  
Crossing Over ◽  
Wild Type ◽  
X Chromosomes ◽  
Unequal Crossing Over ◽  
Quantitative Genetic ◽  
Y Chromosomes ◽  
Homozygous Line ◽  
Minimum Estimate

ABSTRACT Abdominal bristle selection lines (three high and three low) and controls were founded from a marked homozygous line to measure the contribution of sex-linked "mutations" to selection response. Two of the low lines exhibited a period of rapid response to selection in females, but not in males. There were corresponding changes in female variance, in heritabilities in females, in the sex ratio (a deficiency of females) and in fitness, as well as the appearance of a mutant phenotype in females of one line. All of these changes were due to bb alleles (partial deficiencies for the rRNA tandon) in the X chromosomes of these lines, while the Y chromosomes remained wild-type bb+. We argue that the bb alleles arose by unequal crossing over in the rRNA tandon.—A prediction of this hypothesis is that further changes can occur in the rRNA tandon as selection is continued. This has now been shown to occur.—Our minimum estimate of the rate of occurrence of changes at the rRNA tandon is 3 × 10-4. As this is substantially higher than conventional mutation rates, the questions of the mechanisms and rates of origin of new quantitative genetic variation require careful re-examination.

scholarly journals A Genetic Method for Generating Drosophila Eyes Composed Exclusively of Mitotic Clones of a Single Genotype

Genetics ◽  
1999 ◽  
Vol 152 (4) ◽  
pp. 1631-1639 ◽  
Author(s):  
R Steven Stowers ◽  
Thomas L Schwarz
Keyword(s):  
Developmental Stage ◽  
Genetic Screens ◽  
Wild Type ◽  
Phenotypic Analysis ◽  
Standard Methods ◽  
Genetic Method ◽  
Lethal Mutations ◽  
Single Genotype ◽  
Late Developmental Stage ◽  
Fly Eye

Abstract The genetic analysis of a gene at a late developmental stage can be impeded if the gene is required at an earlier developmental stage. The construction of mosaic animals, particularly in Drosophila, has been a means to overcome this obstacle. However, the phenotypic analysis of mitotic clones is often complicated because standard methods for generating mitotic clones render mosaic tissues that are a composite of both mutant and phenotypically normal cells. We describe here a genetic method (called EGUF/hid) that uses both the GAL4/UAS and FLP/FRT systems to overcome this limitation for the Drosophila eye by producing genetically mosaic flies that are otherwise heterozygous but in which the eye is composed exclusively of cells homozygous for one of the five major chromosome arms. These eyes are nearly wild type in size, morphology, and physiology. Applications of this genetic method include phenotypic analysis of existing mutations and F1 genetic screens to identify as yet unknown genes involved in the biology of the fly eye. We illustrate the utility of the method by applying it to lethal mutations in the synaptic transmission genes synaptotagmin and syntaxin.

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