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. 2000 Jun;64(2):281–315. doi: 10.1128/mmbr.64.2.281-315.2000

TABLE 4.

Structural genes of ATP synthase subunits

Genea Proteinb Mutation % Petite productionc Referenced
OLI2, PHO1, ATP6 (mt) Atp6 (F0) Point 20–80 97
OLI1, PHO2, ATP9 (mt) Atp9 (F0) Point 35–49 54
AAP1, ATP8 (mt) Atp8 (F0) Point 50–70 214
 ATP4 (n) b (F0) Disruption 70 229
 ATP5 (n) OSCP (F0) Disruption 40–80 242
 ATP7 (n) d (F0) Deletion High 220
 ATP14 (n) h (F0) Deletion 90 8
 ATP17 (n) f (F0) Disruption 60 285
 ATP18 (n) j (F0 Disruption High 7e
 ATP1 (n) α (F1) Uncharacterized 1 306
Deletion <1 170
 ATP2 (n) β (F1) Uncharacterized 1 306
Deletion <1 170
 ATP3 (n) γ (F1) Disruption 20 228
Deletion 100 170f
 ATP16 (n) δ (F1) Deletion Near 100 106
Deletion 100 170
 ATP15 (n) ɛ (F1) Deletion 25–50 119
Deletion 60 170
a

The genes are carried by either the mitrochondrial (mt) or the nuclear (n) genomes. 

b

The proteins are parts of either the proton channel membrane (F0) or the catalytic (F1) sectors of ATP synthase. 

c

The methods used by the authors do not discriminate between rho and rho0 petites. The values must be interpreted with caution since the basal level of petite production observed in the reference strains was not reported except in the study performed by Lai-Zhang et al. (170): here the wild-type reference strain produces 9% petites. 

d

References are those reporting about petite production. See the text for other relevant references. 

e

Vaillier et al. (309) reported contradictory data concerning ATP18

f

The slight discrepancy between these data might be explained, as suggested by Lai-Zhang et al. (170), by the differences in how the null mutants were constructed, giving rise to a complete or partial deletion.