Site-specific phosphorylation of LRP regulates <i>FLC</i> chromatin looping and flowering.

Abstract

Emerging evidence suggests that multiple RNA recognition motif (RRM)-containing proteins are involved in transcriptional regulation, yet the underlying mechanisms remain largely unclear. Here, we show that the previously uncharacterized LATE-FLOWERING RRM-CONTAINING PROTEIN (LRP) prevents 5'-3' chromatin looping of the key floral repressor gene <i>FLOWERING LOCUS C</i> (<i>FLC</i>) via direct association with its 5' and 3' genomic regions. Loss of <i>LRP</i> function leads to increased 5'-3' gene looping, reduced RNA polymerase II (Pol II) occupancy at the <i>FLC</i> locus, thereby increasing <i>FLC</i> transcription and delaying flowering in <i>Arabidopsis thaliana</i>. Furthermore, site-specific phosphorylation of LRP at serine 17, mediated by the kinase PRP4KA, is essential for LRP protein stability and its function in preventing <i>FLC</i> chromatin looping and Pol II recruitment. Our findings reveal that site-specific phosphorylation of LRP by PRP4KA precludes <i>FLC</i> gene loop formation, constituting a key mechanism for <i>FLC</i> transcriptional repression to ensure timely flowering.