|COX1 deletion ||Deletion of mobile group II intron (intron alpha) from COX1 doubles lifespan and prevents accumulation of senescence-associated DNA concatemer corresponding to this of the mitochondrial genome . Deletion encompassing COX1's intron alpha and its upstream exon abolishes the senescence process entirely . || ||— ||— ||— |
|COX5 deletion ||Disruption of the nuclear COX5 gene delays senescence, increase longevity between 7- and 15-fold (in 30 tested isolates) and the onset of senescence is not associated by accumulation of senescence-specific mtDNA molecules. COX5 deletion results in exclusive use of the alternative respiratory pathway and a decrease in production of reactive oxygen species and the prevention of the accumulation of several senescence-specific mitochondrial DNA molecules . || ||— ||— ||— |
|cyc1 mutation ||cyc1 mutants have a reduced growth rate, a reduced reactive oxygen species production, and are long-lived . || ||— ||— ||— |
|Grisea mutation ||In Grisea (AFUA_1G13190) loss of function mutants, senescence is delayed two-fold .
Grisea disruption extends mean and maximum lifespan by 195 and 210% .
Grisea mutant has altered norphology and defects in formation of female gametangia . || ||+195 ||— ||+210 |
|PaDnm1:ble ||Dnm1 disruption in wild-type extends mean and maximum lifespan by 377 and 329% and its disruption in long-lived grisea mutants prolongs mean and maximum lifespan by 1009 and over 1090% (survival was not followed to the end) . || ||+377 ||— ||+329 |