Temporal Pattern of Bristle Development on Drosophila melanogaster Sternites

1982 ◽  
Vol 35 (6) ◽  
pp. 653 ◽  
Author(s):  
JH Claxton

Bristle development in D. melanogaster can be prevented with X-rays administered prior to the final differentiative divisions of bristle-committed epidermal cells. The epidermal cells are radiationinsensitive if the same dose is given after cell division. By subjecting variously aged early pupae to X-radiation and subsequently scoring bristle numbers in adults, a temporal pattern of radiation insensitivity was established on the abdominal sternites. The pattern is a simple gradient extending anteriorly and medially from the posterior lateral sternite �corners'. The possible significance of this to the origin of bristle spatial patterns is discussed.

Development ◽  
1976 ◽  
Vol 36 (1) ◽  
pp. 109-125
Author(s):  
Robert Ransom

An account of the patterns of clones induced on the head cuticle of Drosophila melanogaster is given. The system was studied using mitotic recombination, induced by X-rays at certain developmental stages. In agreement with the findings of a computer model devised to simulate growth in the head imaginal disc, cuticle clones are found to have a characteristic pattern, weeping round the central, eye-forming part of the disc. The similarity between model and experiment suggests the validity of the model assumption. It is also shown that cuticle clones are not smaller in the posterior of the head, when induced at the developmental stages studied: this is in contrast to clones in the compound eye, where posterior clones are smaller thananterior ones.


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.


1957 ◽  
Vol 3 (2) ◽  
pp. 171-182 ◽  
Author(s):  
S. T. Bayley ◽  
J. R. Colvin ◽  
F. P. Cooper ◽  
Cecily A. Martin-Smith

The primary walls of epidermal cells in Avena coleoptiles ranging in length from 2 to 40 mm. have been studied in the electron and polarizing microscopes and by the low-angle scattering of x-rays. The outer walls of these cells are composed of multiple layers of cellulose microfibrils oriented longitudinally; initially the number of layers is between 10 and 15 but this increases to about 25 in older tissue. Where epidermal cells touch, these multiple layers fuse gradually into a primary wall of the normal type between cells. In these radial walls, the microfibrils are oriented transversely. Possible mechanisms for the growth of the multilayered outer wall during cell elongation are discussed.


1988 ◽  
Vol 89 (1) ◽  
pp. 39-47 ◽  
Author(s):  
C. Gonzalez ◽  
J. Casal ◽  
P. Ripoll

Mutation in the gene merry-go-round (mgr) of Drosophila causes a variety of phenotypic traits in somatic and germinal tissues, such as polyploid cells, metaphasic arrest, postmeiotic cysts with 16 nuclei, and spermatids with four times the normal chromosome content. The most characteristic phenotype is the appearance of mitotic and meiotic figures where all chromosomes are arranged in a circle. Treatment with anti-mitotic drugs and the phenotype of double mutants mgr asp (asp being a mutation altering the spindle) show that these circular figures need a functional spindle for their formation. These abnormal figures are caused by monopolar spindles similar to those observed after different treatments in several organisms. All mutant traits indicate that mgr performs a function necessary for the correct behaviour of centrosomes, thus opening this organelle to genetic analysis.


Development ◽  
1991 ◽  
Vol 113 (4) ◽  
pp. 1357-1364 ◽  
Author(s):  
M. Carmena ◽  
C. Gonzalez ◽  
J. Casal ◽  
P. Ripoll

Most mitotic mutants in Drosophila do not lead to lethality in early development despite the highly abnormal chromosome behaviour that they elicit. This has been explained as being the effect of maternally provided wild-type products. We have tested this hypothesis by studying cuticular clones derived from cells in which there has been loss of a marked Y chromosome due to chromosome nondisjunction in individuals homozygous for the mutation abnormal spindle who are progeny of heterozygous mothers. We have found that the size and frequency of these clones are higher than in control flies. Furthermore, by analysing flies whose female parents have different doses of the asp+ gene, we have found that there is a correlation between the amount of maternally contributed asp+ product and the frequency and size of cuticular clones. We have also estimated the time in development when the first mitotic mistakes take place, i.e. the time when maternal products are no longer sufficient to carry out normal cell division.


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