High impact information on SCL1

• Deletions of PRS2, PRS4, and PRS5 or combinations thereof cause this phenotype [1].
• The wild-type scl1+ gene was isolated by screening subclones of the 35-kb region between TRP5 and LEU1 for restoration of the ts phenotype in an SCL1-1 crl3-2 strain [2].
• In Saccharomyces cerevisiae, the SCL-1 mutation is a dominant suppressor of the cycloheximide-resistant, temperature-sensitive (ts) lethal mutation, crl3 [McCusker and Haber, Genetics 119 (1988a) 303-315] [2].
• The suppressor gene scl1+ of Saccharomyces cerevisiae is essential for growth [2].
• Gene disruption of scl1+ demonstrates that it is an essential gene [2].

Biological context of SCL1

• Addition of a DNA fragment that included the wild-type SCL1 gene to J19 complemented its morphological phenotype [3].
• The scl1+ mRNA is about 900 nt long and encodes an open reading frame of 810 bp [2].
• Southern blot analysis after electrophoretic separation of yeast chromosomal DNAs showed that the PRS2 gene is located in chromosome VII, unlike the PRS1 gene for subunit YC1, is located on chromosome XV [4].

Associations of SCL1 with chemical compounds

• Sequencing of J19 SCL1 showed that the glycine at position 226 in the Scl1 protein had been replaced by asparatic acid, suggesting that this mutation in the protein, a subunit of proteasomes, may be involved in the morphological change [3].

Regulatory relationships of SCL1

• Surprisingly, the overall structure of the PRS2 gene was found to be identical to that of the suppressor scl1+ gene restoring the SCL1-1 mutation that suppresses crl3 cycloheximide-resistant, temperature-sensitive lethality [4].

Analytical, diagnostic and therapeutic context of SCL1

• Molecular cloning of the yeast proteasome PRS2 gene identical to the suppressor gene scl1+ [4].

References