Analysis of yeast mutants defective in a signal transduction pathway from the plasma membrane to the nucleus
| Project/Area Number |
10680671
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | Hiroshima University |
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Principal Investigator |
MIZUTA Keiko Hiroshima University, Faculty of Engineering Associate professor, 工学部, 助教授 (40166012)
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| Co-Investigator(Kenkyū-buntansha) |
水田 啓子 広島大学, 工学部, 助教授 (40166012)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1998: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | membrane traffic / ribosome biogenesis / transcriptional control / ribosomal protein ganes / ribosomal RNA / rRNA processing / ribosome assembly / yeast mutants / リボソーム生合成 |
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| Research Abstract |
We previously reported that a secretory defect caused specific and significant transcriptional repression of both ribosomal protein and rRNA genes. Futher examination using various sec mutants showed that a defect anywhere in the secretory pathway, from a step prior insertion of the nascent peptide into the endoplasmic reticulum to step involved in the formation of the plasma membrane, prevents the continued synthesis of the components of the ribosome. We propose the existence of a signal transduction pathway from the plasma membrane to the nucleus. The purpose of this research is to elucidate the molecular machanism of the signaling.
A plasmid was generated in which the HIS3 gene was driven by the promoter of a ribosomal protein gene. This plasmid was transformed into a yeast temperature sensitive sec mutant, sly1(his3). We isolated several mutants which appeared to be defective in the signaling pathway. One of the mutants, rrs1-1, was cold sensitive and the rrs1-1 mutation greatly reduced transcriptional repression of both rRNA and ribosomal protein genes that is caused by secretory defect. RRS1 is a novel, essential gene encoding a nuclear protein of 203 amino acid residues that is conserved in eukaryotes. Sequence analysis showed that rrs1-1 had only one nucleotide difference, within codon 114, resulting in a stop coden. The truncated rrs1-1 protein appeared to have similar to the wild -type protein. A conditional rrs1-null mutant was constructed by placing RRS1 under the control of the GAL1 promoter. Rrs1 depletion caused defects in processing of pre-RNA and assembly of ribosomal subunits. These results suggest that Rrs1 is essential for ribosome biogenesis and also has an important role in the signaling caused by a secretory defect.
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Report
(3 results)
Research Products
(3 results)
