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".

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.

The role of the genome in the development of the haploid syndrome in Anura

Development ◽  
1966 ◽  
Vol 16 (3) ◽  
pp. 559-568
Author(s):  
Louie Hamilton
Keyword(s):  
Good Evidence ◽  
Contributory Factor ◽  
Diploid Nucleus ◽  
Haploid Nucleus ◽  
Recessive Lethal ◽  
Partial Failure ◽  
Lethal Genes

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.

Functions of the Lymph Gland Cells during the Larval Period in Drosophila

Development ◽  
1957 ◽  
Vol 5 (2) ◽  
pp. 122-133
Author(s):  
H. H. El Shatoury ◽  
C. H. Waddington
Keyword(s):  
Adult Stage ◽  
Larval Period ◽  
Careful Study ◽  
Developmental Effects ◽  
The Individual ◽  
Recent Monograph ◽  
Mutant Genes ◽  
Considerable Body ◽  
Lethal Genes ◽  
Epigenetic Processes

A Considerable body of information has already been accumulated in which a careful study of the morphological effects of a gene in Drosophila has been used to throw light on the epigenetic processes which bring about development. Much of the earlier work of this kind (e.g. Goldschmidt, Waddington) has dealt with mutant genes which produced abnormal adults. More recently a great deal of attention has been paid to the developmental effects of lethal genes which cause the death of the individual before the adult stage is reached. In a recent monograph on this category of genes, Hadorn (1951), who has been one of the most active workers in this field, lays considerable stress on what he calls the phase specificity of the lethals, that is, on the fact that individuals homozygous for a particular lethal usually die at some rather definitely defined stage of their life history.

Biosystematic studies in the Stylidium crassifolium species complex (Stylidiaceae)

1979 ◽  
Vol 27 (1) ◽  
pp. 27 ◽  
Author(s):  
BJ Banyard ◽  
SH James
Keyword(s):  
Species Complex ◽  
Genetic System ◽  
Lethal Gene ◽  
Great Efficiency ◽  
Intermediate Species ◽  
Gene Arrays ◽  
Recessive Lethal ◽  
Tetraploid Form ◽  
Diploid Populations ◽  
Lethal Genes

Stylidium elongatum Benth. (n = 13, 26) and Stylidium crassifolium R. Br. (n = 14, 28) have been restored to specific status and a morphologically intermediate species, Stylidium confluens sp. nov. (n = 14), is described. Polyploid entities in the complex have not been given taxonomic ranks although the tetraploid form of elongatum may be considered worthy of subspecific rank, as it is ecologically distinct and contiguously allopatric to its progenitor and to confluens, forming a buffer between these two diploid entities. Tetraploid populations in crassifolium occur within the distributional range of the diploid. All three species carry recessive lethal gene arrays which eliminate the products of self-pollination with great efficiency and result in crosses between close populations yielding seed more effectively than crosses within populations. There is evidence that interpopulational coadaptation may break down with increasing distance between populations. Polyploidy in crassifolium is probably a conservative response in the genetic system of a species where concentrations of lethal genes in small diploid populations became disadvantageous.

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.

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