The Nuclear Ribonucleoprotein SmD1 Interplays with Splicing, RNA Quality Control, and Posttranscriptional Gene Silencing in Arabidopsis

EMILIE ELVIRA-MATELOT; FLORIAN BARDOU; FEDERICO ARIEL; VINCENT JAUVION; NATHALIE BOUTEILLER; IVAN LEMASSON; JUN CAO; MARTIN CRESPI; HERVÉ VAUCHERET

PLANT CELL

AMER SOC PLANT BIOLOGISTS

Lugar: Rockville; Año: 2016 vol. 28 p. 426 - 438

1040-4651

RNA quality control (RQC) eliminates aberrant RNAs based on their atypical structure, whereas posttranscriptional genesilencing (PTGS) eliminates both aberrant and functional RNAs through the sequence-specific action of short interferingRNAs (siRNAs). The Arabidopsis thaliana mutant smd1b was identified in a genetic screen for PTGS deficiency, revealing theinvolvement of SmD1, a component of the Smith (Sm) complex, in PTGS. The smd1a and smd1b single mutants are viable, butthe smd1a smd1b double mutant is embryo-lethal, indicating that SmD1 function is essential. SmD1b resides in nucleoli andnucleoplasmic speckles, colocalizing with the splicing-related factor SR34. Consistent with this, the smd1b mutant exhibitsintron retention at certain endogenous mRNAs. SmD1 binds to RNAs transcribed from silenced transgenes butnot nonsilenced ones, indicating a direct role in PTGS. Yet, mutations in the RQC factors UPFRAMESHIFT3,EXORIBONUCLEASE2 (XRN2), XRN3, and XRN4 restore PTGS in smd1b, indicating that SmD1 is not essential for butrather facilitates PTGS. Moreover, the smd1b mtr4 double mutant is embryo-lethal, suggesting that SmD1 is essential formRNA TRANSPORT REGULATOR4-dependent RQC. These results indicate that SmD1 interplays with splicing, RQC, andPTGS. We propose that SmD1 facilitates PTGS by protecting transgene-derived aberrant RNAs from degradation by RQC inthe nucleus, allowing sufficient amounts to enter cytoplasmic siRNA bodies to activate PTGS.