Figure 8.

Model for FRY1, XRN2, XRN3, and XRN4 Activity during PTGS.

Shown at left is a simplified model for miRNA biogenesis and action. Normal miRNA maturation requires DCL1, SERRATE, HYL1, and HEN1 and liberates MIRNA loops, miRNA*, and mature miRNAs. miRNAs are exported from the nucleus by HASTY and incorporate into an AGO1-containing complex to direct the cleavage of partially complementary RNAs. MIRNA loops are substrates of both the nuclear XRN2 and XRN3, while 3′ target cleavage products are substrates of the cytoplasmic XRN4. Shown at right is a simplified model for transgene- and virus-induced silencing. Aberrant RNA deriving from transgene transcription and virus replication is converted to double-stranded RNA and processed into siRNAs by RDR6 and SGS3, and DCL2 and DCL4, respectively. siRNAs incorporate into an AGO1-containing complex to direct the cleavage of complementary RNAs. XRN2, XRN3, and XRN4 are endogenous suppressors of PTGS, and we propose that the transgene- and virus-derived aberrant RNAs that trigger PTGS are substrates of these XRNs. At center, FRY1 converts 3′-phosphoadenosine 5′-phosphate (PAP), a toxic byproduct of sulfate assimilation, into 5′ AMP + Pi. Our data, together with those from yeast, predict that XRN levels are regulated through a FRY1-dependent system that keeps PAP, an inhibitor of yeast XRN activity, levels in check. We propose that XRN activities are repressed in fry1 mutant plants, leading to the overaccumulation of aberrant RNAs that trigger PTGS.