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Both transcription and RNA decay are critical for normal gene regulation. Arabidopsis mutants with defects inVARICOSE (VCS ), a decapping complex scaffold protein, lack mRNA decapping and 5′-to-3′ decay. These mutants show either severe or suppressed phenotypes, depending on the Arabidopsis accession. Here, we show that the molecular basis for this variation is theSUPPRESSOR OF VARICOSE (SOV ), a locus that encodes a conserved, cytoplasmically localized RRP44-like RNaseII-domain protein. In vivo RNA decay assays suggest that active forms of this protein carry out decay on mRNA substrates that overlap with those of the decapping complex. Members of this conserved gene family encode proteins lacking the PIN domain, suggesting that SOV is not a functional component of the RNA exosome.

Conserved RNaseII domain protein functions in cytoplasmic mRNA decay and suppresses Arabidopsis decapping mutant phenotypes