mat-3 encodes the APC8 component of the Anaphase Promoting Complex/ Cyclosome (APC/C) (Davis et al., 2002).
mat-3(
ku233) is a weak hypomorphic allele that alters sequences 5 prime to the
mat-3 coding region and appears to slightly reduce
mat-3 expression.
ku233 mutants are fully viable but semi-sterile and have a variety of vulval defects, including variably sized Pn.pxx nuclei and catastrophic failures in the final round of vulval cell divisions. Surprisingly, we found that
mat-3(
ku233) vulval and sterile defects are efficiently suppressed by certain Synthetic Multivulva class B mutations, including
lin-35/Rb,
lin-53/RbAp48,
efl-1/E2F and
dpl-1/DP. Notably, although the class B synMuv gene
lin-36 acts with
lin-35/Rb to inhibit G1-to-S progression (Boxem and van den Heuvel, 2002; Fay et al., 2002), mutations in
lin-36 do not suppress
ku233. The activated Ras allele
let-60(
n1046gf), which is Multivulva, also does not suppress. Therefore, suppression of
ku233 is not a general property of mutations that bypass G1 arrest or that increase Ras signaling/vulval induction, but is instead a specific property of mutations in a subset of SynMuv B genes. Two possible models to explain our findings are that SynMuv B genes repress
mat-3 gene expression, or that the APC/C downregulates SynMuv B protein levels. Overexpression of the zinc finger protein F54C4.3 also suppresses
mat-3(
ku233) defects, but does not behave like a SynMuv class B in that it does not cause a Multivulva phenotype in SynMuv class A backgrounds. Intriguingly, RNAi against F54C4.3 causes many post-embryonic cell division defects. We are further investigating the role of F54C4.3 in cell cycle regulation and its potential relationship to SynMuv gene products.