TABLE 1.
Suppressors of par-2(it5ts) lethality
| RNAi clone | Gene | Embryonic viability (%)a | Domains and description | 
|---|---|---|---|
| Vector | Negative control | 5.5 ± 2.6 | |
| C32E12.2 | Negative control | 8.4 ± 4.5 | |
| F54E7.3 | par-3 | 75.1 ± 5.6 | PDZ domains, component of the anterior PARs | 
| T26E3.3 | par-6 | 29.2 ± 16.1 | PDZ and CRIB domains, component of the anterior PARs | 
| F09E5.1 | pkc-3 | 38.3 ± 19.8 | Kinase domain, component of the anterior PARs | 
| R07G3.1 | cdc-42 | 48.2 ± 27.5 | GTPase domain, activator of the anterior PARs | 
| Y53C12B.3 | nos-3 | 10.0 ± 6.3b | Q/N-rich domain, zf-nanos-type zinc-finger domain, Drosophila Nanos and Xenopus Xcat-2 homolog | 
| F57C2.6 | spat-1 | 15.4 ± 5.5 | Conserved in C. briggsae only | 
| F54F2.5 | ztf-1 | 16.3 ± 5.2 | C2H2-type zinc fingers | 
| Y48A6B.13 | spat-2 | 32.0 ± 8.8 | Conserved in C. briggsae only | 
| Y43E12A.1c | cyb-2.1 cyb-2.2 | 59.3 ± 6.1 | Cyclin B homologs | 
| W02A2.1 | fat-2 | 22.7 ± 9.6 | Fatty acid desaturase | 
| ZC64.3 | ceh-18 | 20.9 ± 7.0 | POU-class homeodomain transcription factor | 
| T13H2.5 | spat-3 | 50.9 ± 12.1 | C3HC4-type RING-finger domain and Q/N-rich domain | 
| ZK20.5 | rpn-12 | 48.0 ± 18.5 | Component of the 26S proteasome non-ATPase regulatory particle | 
| T06D8.8 | rpn-9 | 22.9 ± 6.6 | Component of the 26S proteasome non-ATPase regulatory particle | 
| B0205.3 | rpn-10 | 25.4 ± 10.3 | Component of the 26S proteasome non-ATPase regulatory particle | 
Suppressors of par-2 (it5ts) lethality were determined by feeding RNAi clones to animals at the L1 stage. All of these clones were not identified in the genomewide screen; see text and materials and methods for details.
The value corresponds to the average percentage of embryos that hatched over the total number of embryos ± standard deviation over eight assays.
Although nos-3 was not found to suppress par-2 in this particular assay, it was included as a suppressor of par-2 since it suppressed all of the par-2 phenotypes in other assays.
Clone Y43E12A.1 might disrupt the function of both cyb-2.1 and cyb-2.2 since these two genes are 95% identical at the nucleic acid level.