Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.639245
Title: Genetic change in living cells
Author: Tippins, R. S.
Awarding Body: University College of Swansea
Current Institution: Swansea University
Date of Award: 1980
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Abstract:
The major aim of this project has been the study of the action of mutagens upon yeast cells at discrete stages of the cell cycle. To provide a sufficiently large population of cells at appropriate stages of the mitotic division cycle it has been necessary to develop the use of the zonal rotor for this purpose. After treatment with a range of physical and chemical mutagens cyclic variations were observed in the induction of a number of genetic end points i.e. mitotic recombination (both reciprocal and non- reciprocal), mutation (both base substitution and frameshift) and mitotic aneuploidy. In general, physical mutagens were found to give maximum induction of these genetic end points in GI, whereas the chemical mutagens predominantly had their maximal effect upon S phase cells. Control experiments have indicated that the observed GI sensitivity of yeast cells to radiation cannot be attributed to cell size differences (cytoplasmic shielding). However the budding resistance of S and G2 cells required a functional RAD 50 gene together with the close association of sister chromatids. A sister strand exchange post-replication repair mechanism has been proposed to account for budding repair of radiation damage. The increased sensitivity of S phase cells to chemical mutagens may occur due to differential uptake. Larger amounts of labelled EMS were taken into yeast cells during S phase, when possibly the DNA of the cells was more exposed. The observed association between the maximum induction of lethality and the induction of the various genetic end points has led to the conclusion that similar DNA lesions can lead to different genetic consequences during the cell cycle. However, the situation may be complicated by data which shows that caffeine reduces gene conversion whilst increasing base substitution mutation in S phase after nitrous acid exposure. This indicates that error-prone repair and mitotic gene conversion may compete for similar DNA lesions. Indirect evidence has also been presented which indicates that error-prone repair in yeast may be constitutive whereas error-free repair may be inducible. Cell populations of stationary and G1 phase cells were found to be distinguishable on the basis of their radiosensitivity. This has been taken as support for the hypothesis that stationary phase cells are outside the mitotic cell cycle in CO phase.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.639245  DOI: Not available
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