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Evolution of altered signaling in th...
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Shumway, Laurence Alan.
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Evolution of altered signaling in the yeast Saccharomyces cerevisiae.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Evolution of altered signaling in the yeast Saccharomyces cerevisiae./
作者:
Shumway, Laurence Alan.
面頁冊數:
187 p.
附註:
Adviser: Andrew Wood Murray.
Contained By:
Dissertation Abstracts International68-02B.
標題:
Biology, Genetics. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3251315
Evolution of altered signaling in the yeast Saccharomyces cerevisiae.
Shumway, Laurence Alan.
Evolution of altered signaling in the yeast Saccharomyces cerevisiae.
- 187 p.
Adviser: Andrew Wood Murray.
Thesis (Ph.D.)--Harvard University, 2007.
In this dissertation I will present the evolution and characterization of a genetically complex trait. The trait is defined by fluctuations in a fluorescent FUS1 transcriptional reporter. The trait was evolved by an iterated, alternating selection scheme; cells were alternately selected to have either high or low fluorescence. The fluctuations occur in the absence of external stimulus.Subjects--Topical Terms:
1017730
Biology, Genetics.
Evolution of altered signaling in the yeast Saccharomyces cerevisiae.
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In this dissertation I will present the evolution and characterization of a genetically complex trait. The trait is defined by fluctuations in a fluorescent FUS1 transcriptional reporter. The trait was evolved by an iterated, alternating selection scheme; cells were alternately selected to have either high or low fluorescence. The fluctuations occur in the absence of external stimulus.
520
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This reporter is a proxy for activation of the pheromone response pathway in wild-type Saccharomyces cerevisiae. Key components of the pheromone response pathway including the pheromone receptor, its associated trimeric G-protein, a scaffolding protein, and effector kinase, are non-essential for the trait. The components of the Cdc42-dependent invasive growth MAPK cascade are essential for the fluctuations. Four mutations of strong effect instruct this trait, two of which were identified in this study. A third mutation can be effectively phenocopied by deletion of key components of the osmotolerance pathway. Our model proposes that the mutations support a positive signal that stimulates the invasive growth pathway. One of the identified mutations, a loss of function mutation in an invasive growth transcription co-factor, TEC1, permits this signal to be directed to a reporter for the mating pathway.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3251315
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