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Published on May 8, 2009; 10.1104/pp.109.137448

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Received February 21, 2009
Accepted May 3, 2009

FRIGIDA delays flowering in Arabidopsis via a co-transcriptional mechanism involving direct interaction with the nuclear cap binding complex

Nuno Geraldo , Isabel Baurle , Shin-ichiro Kidou , Xiangyang Hu , and Caroline Dean *

Department of Cell & Developmental Biology, John Innes Centre, Colney Lane, Norwich UK NG, IB, XH, CD), Cryobiosystem Research Center, Iwate University, Morioka, Iwate 020-8550, Japan (SK)

* Corresponding author; email: caroline.dean{at}bbsrc.ac.uk.

A major determinant of flowering time in natural Arabidopsis thaliana variants is FRIGIDA (FRI). FRI up-regulates expression of the floral repressor FLOWERING LOCUS C (FLC), thereby conferring a vernalization requirement and a winter annual habit. FRI encodes a novel nuclear protein with no conserved domains except for two coiled coil regions. A mutation in the large subunit of the nuclear cap binding complex (CBC) suppresses FRI activity so we have explored the connection between FRI and the nuclear CBC in order to gain further insight into FRI biochemical activity. Mutations in the small subunit of the CBC (CBP20) also suppress FRI up-regulation of FLC. CBP20 interacted directly with FRIGIDA in yeast and in planta and this association of FRI with the 5' cap was reinforced by an RNA ligase-mediated RACE assay that showed FRI decreased the proportion of FLC transcripts lacking a 5' cap. Loss of CBP20 resulted in very low FLC mRNA levels and an increased proportion of unspliced FLC transcripts. FRI compensated for CBP20 loss, partially restoring FLC levels and normalizing the unspliced/spliced transcript ratio. Our data suggest that FRI up-regulates FLC expression through a co-transcriptional mechanism involving direct physical interaction with the nuclear CBC with concomitant effects on FLC transcription and splicing.






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