期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2010
卷号：107
期号：36
页码：15981-15985
DOI：10.1073/pnas.1007060107
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Both transcription and RNA decay are critical for normal gene regulation. Arabidopsis mutants with defects in VARICOSE (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 the SUPPRESSOR 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.
