Figure 8. Speculative model of genetic interactions involving the
paqr-1 and
paqr-2 genes. This model could explain the observed genetic interactions in the following way: 1)
paqr-1 or
paqr-2 are synthetic lethal with
sbp-1 (or
fat-6) due to reduced fatty acid synthesis/ TAG storage (reduced substrate supply) and reduced fatty acid oxidation, leading to ATP shortage; 2)
paqr-2;
nhr-49 is lethal because two redundant pathways regulating fatty acid oxidation are impaired; 3)
paqr-2;
aak-2 are healthier than the
paqr-2 single mutant because the
aak-2 mutation causes increased lipolysis, thus providing more fatty acids for energy production; and 4)
paqr-2 nhr-80 double mutants have decreased fatty acid desaturation (since
nhr-80 is a positive regulator of
fat-5 and
fat-7), which may result in improved membrane fluidity at 15uC. Mutations in genes highlighted in red were synthetic lethal with
paqr-2 while those in green produced genetic rescues.