FLOWERING LOCUS K and C-terminal domain phosphatase-like 1 cooperate to repress FLOWERING LOCUS C and promote flowering in Arabidopsis thaliana
Abstract
Successful plant reproduction largely relies on the timely transition to flowering, a developmental switch orchestrated by intertwined genetic regulatory networks that integrate internal and environmental cues. In Arabidopsis thaliana, a central regulator of this process is the floral repressor FLOWERING LOCUS C (FLC), whose expression is exquisitely modulated by components of the autonomous pathway through transcriptional and co-transcriptional mechanisms. The KH-domain protein FLOWERING LOCUS K (FLK) downregulates FLC splicing. Consequently, flk mutants flower late because of high FLC expression levels. In this study, we show that FLK functionally interacts with C-TERMINAL DOMAIN PHOSPHATASE-LIKE 1 (CPL1) to promote flowering. CPL1 dephosphorylates the C-terminal domain (CTD) of RNA polymerase II (RNAP II), contributing to the repression of FLC transcription. In line with this, cpl1 mutants flower moderately late due to a mild increase in FLC levels. Our genetic and molecular analyses indicate that the lack of CPL1 synergistically enhances FLC expression and flowering time in the flk background. The physical interaction between FLK and CPL1 might support this scenario. We also found that, in addition to flowering, FLK and CPL1 interact in response to abiotic stress. These observations are consistent with our transcriptomic analysis and suggest the existence of additional common target genes beyond FLC. Our findings offer new perspectives on FLC co-transcriptional regulation, and the coordination between flowering and stress responses.
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BibTeX
@article{rodriguezcazorla2026flowering,
title = {{FLOWERING LOCUS K and C-terminal domain phosphatase-like 1 cooperate to repress FLOWERING LOCUS C and promote flowering in Arabidopsis thaliana}},
author = {Encarnación Rodríguez-Cazorla and Sara Ramos and Elena Monfort and Héctor Candela and Juan-José Ripoll and Antonio Martínez-Laborda and Antonio Vera},
journal = {Frontiers in Plant Science},
year = {2026},
month = nov,
doi = {10.3389/fpls.2026.1940925},
url = {https://www.frontiersin.org/articles/10.3389/fpls.2026.1940925},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - FLOWERING LOCUS K and C-terminal domain phosphatase-like 1 cooperate to repress FLOWERING LOCUS C and promote flowering in Arabidopsis thaliana
AU - Encarnación Rodríguez-Cazorla
AU - Sara Ramos
AU - Elena Monfort
AU - Héctor Candela
AU - Juan-José Ripoll
AU - Antonio Martínez-Laborda
AU - Antonio Vera
PY - 2026
DA - 2026/11/03
JO - Frontiers in Plant Science
DO - 10.3389/fpls.2026.1940925
UR - https://www.frontiersin.org/articles/10.3389/fpls.2026.1940925
AB - Successful plant reproduction largely relies on the timely transition to flowering, a developmental switch orchestrated by intertwined genetic regulatory networks that integrate internal and environmental cues. In Arabidopsis thaliana, a central regulator of this process is the floral repressor FLOWERING LOCUS C (FLC), whose expression is exquisitely modulated by components of the autonomous pathway through transcriptional and co-transcriptional mechanisms. The KH-domain protein FLOWERING LOCUS K (FLK) downregulates FLC splicing. Consequently, flk mutants flower late because of high FLC expression levels. In this study, we show that FLK functionally interacts with C-TERMINAL DOMAIN PHOSPHATASE-LIKE 1 (CPL1) to promote flowering. CPL1 dephosphorylates the C-terminal domain (CTD) of RNA polymerase II (RNAP II), contributing to the repression of FLC transcription. In line with this, cpl1 mutants flower moderately late due to a mild increase in FLC levels. Our genetic and molecular analyses indicate that the lack of CPL1 synergistically enhances FLC expression and flowering time in the flk background. The physical interaction between FLK and CPL1 might support this scenario. We also found that, in addition to flowering, FLK and CPL1 interact in response to abiotic stress. These observations are consistent with our transcriptomic analysis and suggest the existence of additional common target genes beyond FLC. Our findings offer new perspectives on FLC co-transcriptional regulation, and the coordination between flowering and stress responses.
SN - 1664-462X
ER -