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Studies on the cell cycle in Paramecium tetraurelia Rasmussen, Colin Dale
Abstract
Several aspects o-f the cell cycle in Parameciurn were studied using the temperature-sensitive mutations cc1 and cc2, and the recessive gene mutation tamG. Cell cycle progression can be blocked by the cc1 defect up to 0.72 of the cell cycle. There was no progression through the cell cycle at the restrictive temperature, nor excess delay o-f cell division once cells were returned to permissive conditions. The cc1 defect also reversibly inhibits macronuclear DNA synthesis throughout the cell cycle. Macronuclear DNA synthesis is not required for cell division past 0.72 of the cell cycle. Downward regulation of cell mass was examined. Cell mass is regulated by the concerted action of two mechanisms. First, the rate of growth becomes limited by gene dosage when cell mass increases. Second, the cell cycle is shortened when initial cell mass is increased, at the expense of G1. Cells with an initial cell mass greater than 120% of normal initial mass have a cell cycle duration equal to the normal length of S + nuclear division. Both cell mass and parental DNA content influence the timing of DNA synthesis initiation. As initial cell mass increases, the length of G1 decreases. When initial cell mass exceeds the normal value at the start of S, DNA synthesis begins immediately after fission, without a G1 period. G1 DNA content has no effect on the timing of DNA synthesis initiation. However, cells with low parental DNA content appear to enter S phase earlier than cells with high parental DNA content. A simple computer simulation model has been developed which consistent with the experimental observations. The model is based the unstable inhibitor model of Yeas et al. <1945>.
Item Metadata
Title |
Studies on the cell cycle in Paramecium tetraurelia
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
1984
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Description |
Several aspects o-f the cell cycle in Parameciurn were studied using the temperature-sensitive mutations cc1 and cc2, and the recessive gene mutation tamG.
Cell cycle progression can be blocked by the cc1 defect up to 0.72 of the cell cycle. There was no progression through the cell cycle at the restrictive temperature, nor excess delay o-f cell division once cells were returned to permissive conditions. The cc1 defect also reversibly inhibits macronuclear DNA synthesis throughout the cell cycle. Macronuclear DNA synthesis is not required for cell division past 0.72 of the cell cycle.
Downward regulation of cell mass was examined. Cell mass is regulated by the concerted action of two mechanisms. First, the rate of growth becomes limited by gene dosage when cell mass increases. Second, the cell cycle is shortened when initial cell mass is increased, at the expense of G1. Cells with an initial cell mass greater than 120% of normal initial mass have a cell cycle duration equal to the normal length of S + nuclear division.
Both cell mass and parental DNA content influence the timing of DNA synthesis initiation. As initial cell mass increases, the length of G1 decreases. When initial cell mass exceeds the normal value at the start of S, DNA synthesis begins immediately after fission, without a G1 period. G1 DNA content has no effect on the timing of DNA synthesis initiation. However, cells with low parental DNA content appear to enter S phase earlier than cells with high parental DNA content.
A simple computer simulation model has been developed which consistent with the experimental observations. The model is based the unstable inhibitor model of Yeas et al. <1945>.
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Genre | |
Type | |
Language |
eng
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Date Available |
2010-05-16
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0096166
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.