Table 1.
Category | No. of ORFs | No. induced | No. repressed | % of total |
---|---|---|---|---|
Chaperone/heat shock | 31 | 30 | 1 | 4.4 |
Protein synthesis | 77 | 1 | 76 | 11 |
Mitochondrial/energy generationa | 36 | 1 | 35 | 5 |
Metabolismb | 97 | 29 | 68 | 14 |
Transcription | 18 | 7 | 11 | 2.5 |
RNA processing | 6 | 5 | 1 | 0.8 |
DNA replication, recombination, repair, structure | 18 | 3 | 15 | 2.5 |
Protein modification | 11 | 1 | 10 | 1.6 |
Protein degradation | 7 | 5 | 2 | 1 |
Vesicular transport | 11 | 4 | 7 | 1.6 |
Signaling | 7 | 1 | 6 | 1 |
Cell wall/structural | 12 | 2 | 10 | 1.7 |
Mating/budding | 4 | 0 | 4 | 0.6 |
Cell cycle | 4 | 2 | 2 | 0.6 |
Other | 5 | 1 | 4 | 0.7 |
Uncharacterized ORFs | 360 | 148 | 212 | 51 |
Total | 704 | 240 | 464 | 100% |
Twenty-three small molecule transporters, 74 involved in the metabolism of amino acids (20), carbohydrates (17), nucleotides (15), lipids/fatty acids (17), phosphate (2), and others (3).
Cells disrupted for SRP function rapidly lose the ability to grow on nonfermentable carbon sources, i.e., unless selective pressure is applied to the contrary, they become rho−. The reason for this tendency is unknown; it is not a prerequisite for survival as cells can be forced to retain mitochondrial function if they are continuously grown on nonfermentable carbon sources. We previously characterized protein translocation defects of rho− strains following SRP-depletion and found that these strains can also adapt (Ogg et al., 1992). We therefore conclude that a loss of respiratory function is not responsible for adaptation.