Table 3. Summary of Rpn11 phenotypes.
The Table shows a general summary of the phenotypes observed for the rpn11 mutants detailed in this study.
| Growth phenotypes | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| Mutant | Region | Proteasome structural defects | PolyUb–conjugate accumulation | Sensitivity to temperature | Can | CHX | UV | MMS | Growth on glycerol | Mitochondria structural defects |
| mpr1-1 | C-terminus* | + | + | + | − | − | − | + | − | + |
| mpn | N-terminus† | − | + | + | + | + | + | + | + | − |
| mpr1-1 [mpn] | Intragene complementation‡ | − | +/− | − | − | + | − | |||
| mpr1-1 [Rpn8] | Extragene complementation§ | − | − | − | + | − | + | |||
* The mpr1-1 mutant results in a frameshift and truncation in the final (C-terminal) 30 amino acids of Rpn11.
† A general summary of phenotypes common to single-site substitutions at key residues that define the MPN+ putative metalloprotease motif (the signature EHxHSD consensus sequence) of Rpn11.
‡ Most phenotypes associated with either mutant are suppressed upon intragene complementation of naturally abundant mpn-mutated rpn11 expressed in an mpr1-1 background.
§ Extragene complementation of mpr1-1 by overexpression of RPN8. Proteasomal and proteolytic defects are corrected, but not mitochondrial or respiratory defects.