Abstract
Correct gene expression requires tight RNA quality control both at transcriptional and post-transcriptional levels. Using a splicing-defective allele of PASTICCINO2 (PAS2), a gene essential for plant development, we isolated suppressor mutations modifying pas2-1 mRNA profiles and restoring wild-type growth. Three suppressor of pas2 (sop) mutations modified the degradation of mis-spliced pas2-1 mRNA species, allowing the synthesis of a functional protein. Cloning of the suppressor mutations identified the core subunit of the exosome SOP2/RRP4, the exosome nucleoplasmic cofactor SOP3/HEN2 and a novel zinc-finger protein SOP1 that colocalizes with HEN2 in nucleoplasmic foci. The three SOP proteins counteract post-transcriptional (trans)gene silencing (PTGS), which suggests that they all act in RNA quality control. In addition, sop1 mutants accumulate some, but not all of the misprocessed mRNAs and other types of RNAs that are observed in exosome mutants. Taken together, our data show that SOP1 is a new component of nuclear RNA surveillance that is required for the degradation of a specific subset of nuclear exosome targets.
Highlights
There is an error in the third subsection of the Results section, entitled “sop1 suppresses the splicing-defective pas2-1 allele”
The sentence “For this purpose, we introgressed sop1-5, a knock-out allele, that harbours a T-DNA insertion in the At5g21580 locus which encodes the SOP1 protein (see below), into the original pas2-1 mutant as well as into pas1-2, pas2-4 and pas3-1 mutants [16,21,22].” should read: “For this purpose, we introgressed sop1-5, a knock-out allele, that harbours a T-DNA insertion in the At1g21580 locus which encodes the SOP1 protein (see below), into the original pas2-1 mutant as well as into pas1-2, pas2-4 and pas3-1 mutants [16,21,22].”
Summary
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