Table 1. Impact of gene deletions on growth in S. cerevisiae.
| Defined complete Glc
|
Defined minimal Glc
|
Defined minimal Ace
|
Defined minimal Eth
|
||
|---|---|---|---|---|---|
| Gene | (in silico/in vivo) | (in silico/in vivo) | (in silico/in vivo) | (in silico/in vivo) | Refs. (for minimal media) |
| ACO1 | (+/+) | (—/—) | 44 | ||
| CDC19* | (+/—) | (+/—) | 45 | ||
| CIT1 | (+/+) | (+/+) | 46 | ||
| CIT2 | (+/+) | (+/+) | 46 | ||
| CIT3 | (+/+) | ||||
| DAL7 | (+/+) | (+/+) | (+/+) | (+/+) | 47 |
| ENO1 | (+/+) | ||||
| ENO2† | (+/—) | (+/—) | |||
| FBA1‡ | (+/—) | (+/—) | |||
| FBP1 | (+/+) | (+/+) | (—/—) | 48, 49 | |
| FUM1 | (+/+) | ||||
| GLK1 | (+/+) | ||||
| GND1§ | (+/—) | (+/—) | |||
| GND2 | (+/+) | ||||
| GPM1¶ | (+/—) | (+/—) | |||
| GPM2 | (+/+) | ||||
| GPM3 | (+/+) | ||||
| HXK1 | (+/+) | ||||
| HXK2 | (+/+) | ||||
| ICL1 | (+/+) | (+/+) | 50 | ||
| IDH1 | (+/+) | (+/+) | 51 | ||
| IDH2 | (+/+) | (+/+) | 51 | ||
| IDP1 | (+/+) | (+/+) | 52 | ||
| IDP2 | (+/+) | (+/+) | 52 | ||
| IDP3 | (+/+) | ||||
| KGD1 | (+/+) | (+/+) | 53 | ||
| KGD2 | (+/+) | (+/+) | 53 | ||
| LPD1 | (+/+) | ||||
| LSC1 | (+/+) | (+/+) | (+/+) | 54 | |
| LSC2 | (+/+) | (+/+) | (+/+) | 54 | |
| MAE1 | (+/+) | (+/+) | (+/+) | 45 | |
| MDH1 | (+/+) | (+/+) | (+/—) | 55 | |
| MDH2 | (+/+) | (+/—) | (+/—) | 55 | |
| MDH3 | (+/+) | ||||
| MLS1 | (+/+) | (+/+) | (+/+) | (+/+) | 47 |
| OSM1 | (+/+) | ||||
| PCK1 | (+/+) | ||||
| PDC1 | (+/+) | (+/+) | 56 | ||
| PDC5 | (+/+) | (+/+) | 56 | ||
| PDC6 | (+/+) | (+/+) | 56 | ||
| PFK1 | (+/+) | (+/+) | 57 | ||
| PFK2 | (+/+) | (+/+) | 57 | ||
| PGI1‡, ∥ | (+/—) | (+/—) | 58 | ||
| PGK1‡ | (+/—) | (+/—) | |||
| PGM1 | (+/+) | (+/+) | 59 | ||
| PGM2 | (+/+) | (+/+) | 59 | ||
| PYC1 | (+/+) | (+/+) | (+/—) | (+/—) | 60 |
| PYC2 | (+/+) | ||||
| PYK2 | (+/+) | (+/+) | (+/+) | 45, 55 | |
| RKI1 | (—/—) | ||||
| RPE1 | (+/+) | ||||
| SOL1 | (+/+) | ||||
| SOL2 | (+/+) | ||||
| SOL3 | (+/+) | ||||
| SOL4 | (+/+) | ||||
| TAL1 | (+/+) | (+/+) | 61 | ||
| TDH1 | (+/+) | ||||
| TDH2 | (+/+) | ||||
| TDH3 | (+/+) | ||||
| TKL1 | (+/+) | (+/+) | 61 | ||
| TKL2 | (+/+) | ||||
| TPI1‡, ** | (+/—) | ||||
| ZWF1 | (+/+) | (+/+) | 61 |
Growth on different media was considered, including defined complete medium with glucose (Glc) as the carbon source, and minimal medium with Glc, ethanol (Eth), or acetate (Ace) as the carbon source.
+/—, growth/no growth.
The isoenyzme Pyk2p is glucose repressed and cannot sustain growth on glucose
ENO1 plays central role in gluconeogenesis whereas ENO2 is used in glycolysis (66)
Model predicts single deletion mutant to be (highly) growth retarded
Gnd1p accounts for 80% of the enzyme activity. A mutant deleted in GND1 accumulates gluconate-6-phosphate, which is toxic to the cell (62)
The isoenzymes Gpm2p and Gpm3p cannot sustain growth on glucose. They show residual in vivo activity only when they are expressed from a foreign promoter (65)
Different hypotheses exist for why Pgilp-deficient mutants do not grow on glucose, e.g., the pentose phosphate pathway in S. cerevisiae is insufficient to support growth and cannot supply the EMP pathway with sufficient amounts of fructose-6-phosphate and glyceraldehydes-3-phosphate (64)
Growth of single deletion mutant is inhibited by glucose (63)