The spd (sporulation derepressed) mutants of Saccharomyces cerevisiae appear to have lost some of the nitrogen source repression of sporulation but remain subject to glucose repression. In media containing acetate, glycerol or pyruvate as the sole carbon source, these mutants sporulate profusely, a phenotype referred to as hypersporulation (Dawes and Calvert, 1984). This hypersporulation phenotype is also characteristic of mutants in the cAMP signal pathway which have low intracellular levels of cAMP e.g. cdc25, ras2, cdc35, yet the spdl mutants are not allelic to any of these genes. A 4.8 kb DNA sequence on a multicopy plasmid was isolated by its ability to restore growth and inhibit hypersporulation of spdl mutants on YEPG medium. Using the technique of Tn5 transposon mutagenesis, an area of 1.7 - 2.6 kb within the sequence was shown to be responsible for the above effects. The sequence hybridized to chromosome VIII indicating that it was an extragenic suppressor of the SPDI gene, which is situated on chromosome XV. Cells disrupted within the complementing region of the sequence grew more slowly than the corresponding wild-type on YEPD media. On complete media containing ethanol, glycerol or acetate as the sole carbon source, the disruptant did not grow at 30°C but grew at 26°C although at a slower rate than the corresponding wild-type. Diploids ho-mozygous for the above disruption sporulated to a much lesser extent than the corresponding wild-type cells and showed a significantly slower rate of respiration than the wild-type on both YEPD and YEPG media. DNA sequence analysis of the complementing region of the above sequence showed that it was identical to the SCH9 gene which was isolated by Toda et al., (1988).
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:660894 |
| Date | January 1990 |
| Creators | Ramage, Anne Donaldson |
| Publisher | University of Edinburgh |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://hdl.handle.net/1842/16922 |
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