C-TERMINAL DOMAIN PHOSPHATASE-LIKE 1 promotes flowering with TAF15b by repressing the floral repressor gene FLOWERING LOCUS C

Arabidopsis TATA-BINDING PROTEIN-ASSOCIATED FACTOR15b (TAF15b) is a plant-specific component of the transcription factor IID complex. TAF15b is involved in the autonomous pathway for flowering and represses the transcription of FLOWERING LOCUS C (FLC), a major floral repressor in Arabidopsis. While...

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Veröffentlicht in:Molecules and cells 2024, 47(1), , pp.1-7
Hauptverfasser: Kyung, Jinseul, Jeong, Daesong, Eom, Hyunjoo, Kim, Jeesoo, Kim, Jong-Seo, Lee, Ilha
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Sprache:eng
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Zusammenfassung:Arabidopsis TATA-BINDING PROTEIN-ASSOCIATED FACTOR15b (TAF15b) is a plant-specific component of the transcription factor IID complex. TAF15b is involved in the autonomous pathway for flowering and represses the transcription of FLOWERING LOCUS C (FLC), a major floral repressor in Arabidopsis. While components of the autonomous flowering pathway have been extensively studied, scant attention has been directed toward elucidating the direct transcriptional regulators responsible for repressing FLC transcription. Here, we demonstrate that C-TERMINAL DOMAIN PHOSPHATASE-LIKE 1 (CPL1) is a physical and functional partner of TAF15b, playing a role in FLC repression. CPL1 is a protein phosphatase that dephosphorylates the C-terminal domain of RNA polymerase II (Pol II). Through the immunoprecipitation and mass spectrometry technique, we identified CPL1 as an interacting partner of TAF15b. Similar to taf15b, the cpl1 mutant showed a late-flowering phenotype caused by an increase in FLC levels. Additionally, the increase in cpl1 was correlated with the enrichment of phosphorylated Pol II in the FLC chromatin, as expected. We also discovered that CPL1 and TAF15b share additional common target genes through transcriptome analysis. These results suggest that TAF15b and CPL1 cooperatively repress transcription through the dephosphorylation of Pol II, especially at the FLC locus.
ISSN:1016-8478
0219-1032
0219-1032
DOI:10.1016/j.mocell.2024.100114