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. Author manuscript; available in PMC: 2021 Jan 6.
Published in final edited form as: Dev Cell. 2020 Jan 6;52(1):88–103.e18. doi: 10.1016/j.devcel.2019.12.005

Table 1.

CK1δ suppressors are in transcription termination components and unc-44 / Ankyrin.

gene # of alleles cellular process mutation
kin-20 4 Casein kinase 1 delta Missense, revertants
kin-19 1 Casein kinase 1 alpha Missense
ssup-72 5 Phosphatase for RNAP II CTD Missense
pinn-1 3 Prolyl isomerase for RNAP II CTD Missense and null
pcf-11 1 3’ pre-mRNA processing Missense
cpsf-4 3 Cleavage polyadenylation factor complex Missense
pfs-2 1 Cleavage polyadenylation factor complex Missense
ctr-9 3 Elongation/termination, Paf1 complex Missense
cdc-73 1 Elongation/termination, Paf1 complex Splice acceptor, null
zfp-3 7 Likely RNA pol II complex Missense and nulls
rpb-2 5 RNAP II subunit B Missense
cdk-8 1 Mediator and RNA pol II complex Missense
unc-44 4 Ankyrin, cytoskeletal Missense
Unconfirmed hits
zfp-3 1 Likely RNA pol II complex Intronic mutation
swd-2.2 1 Set1/COMPASS complex Missense
pinn-1 1 Prolyl isomerase for RNAP II CTD Intronic mutation

The genes identified in the kin-20 suppressor screen. Four kin-20(ox423) revertants and pseudo-revertants were identified, indicating that the screen was approaching saturation. kin-19(ox689) is a predicted hypermorphic mutation of casein kinase 1α, a CK1 isoform closely related to CK1δ. unc-44 alleles are found in the polyadenylation site (ox685, ox832, ox833) and within a conserved intron upstream of the polyadenylation site (ox686). All other mutations are in components of the RNA polymerase II complex, most with functions in transcription termination. The same mutation, pfs-2(R158Q), was identified previously in a neuronal branching suppressor screen (Van Epps et al., 2010).