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Regulated arrest of cell proliferation mediated by yeast prt1 mutations
P J Hanic-Joyce1, G C Johnston, R A Singer
1Department of Microbiology, Dalhousie University, Halifax, Nova Scotia, Canada.
Abstract:
Several temperature-sensitive cell-division-cycle (cdc) mutations differentially affect the regulatory step for cell proliferation in the yeast. Saccharomyces cerevisiae, including one mutation termed cdc63-1, which resides in a previously known gene called PRT1. Other mutations in the PRT1 gene have been shown by others to affect an initiation step in protein synthesis. Here we show that at the appropriate nonpermissive temperature each prt1 mutation can produce a uniform and concerted arrest of cell division; the prt1-1 mutation, like cdc63-1, is shown to arrest cells specifically at the regulatory step for cell proliferation. This response of cessation of cell division is different from the response of cells to an equivalent limitation of protein synthesis using cycloheximide or verrucarin A, which implies that the PRT1 gene product could separately influence both cellular growth via protein synthesis and events in the regulation of cell proliferation.
Insights
Mutations in the PRT1 gene of Saccharomyces cerevisiae arrest cell division at a regulatory step. This suggests the PRT1 gene product influences both protein synthesis and cell proliferation regulation.
Area of Science:
- Molecular Biology
- Cell Biology
- Yeast Genetics
Background:
- The PRT1 gene in Saccharomyces cerevisiae is known to be involved in protein synthesis initiation.
- Cell-division-cycle (cdc) mutations can disrupt cell proliferation regulation.
- The specific role of PRT1 in cell cycle regulation was not fully understood.
Purpose of the Study:
- To investigate the role of PRT1 mutations in cell cycle regulation.
- To determine if PRT1 mutations affect the regulatory step of cell proliferation.
- To differentiate the effects of PRT1 mutations from general protein synthesis inhibition.
Main Methods:
- Utilizing temperature-sensitive prt1 mutations in Saccharomyces cerevisiae.
- Observing cell division arrest at nonpermissive temperatures.
- Comparing the effects of prt1 mutations with protein synthesis inhibitors like cycloheximide and verrucarin A.
Main Results:
- Specific prt1 mutations, including prt1-1 and cdc63-1, cause a uniform cell division arrest at the regulatory step.
- This cell division arrest is distinct from the effects of general protein synthesis inhibition.
- The PRT1 gene product appears to have a dual role in cellular processes.
Conclusions:
- The PRT1 gene product plays a critical role in regulating cell proliferation distinct from its role in protein synthesis.
- PRT1 influences both cellular growth through protein synthesis and the regulation of cell division.
- Understanding PRT1's function provides insights into the coordination of cell growth and division.