Gibberellin Signaling through RGA Suppresses GCN5 Effects on Arabidopsis Developmental Stages

Christina Balouri, Stylianos Poulios, Dimitra Tsompani, Zoe Spyropoulou, Maria-Christina Ketikoglou, Athanasios Kaldis, John H. Doonan, Konstantinos E. Vlachonasios*

*Awdur cyfatebol y gwaith hwn

Allbwn ymchwil: Cyfraniad at gyfnodolynErthygladolygiad gan gymheiriaid

1 Dyfyniad (Scopus)

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Histone acetyltransferases (HATs) modify the amino-terminal tails of the core histone proteins via acetylation, regulating chromatin structure and transcription. GENERAL CONTROL NON-DEREPRESSIBLE 5 (GCN5) is a HAT that specifically acetylates H3K14 residues. GCN5 has been associated with cell division and differentiation, meristem function, root, stem, foliar, and floral development, and plant environmental response. The flowers of gcn5 plants display a reduced stamen length and exhibit male sterility relative to the wild-type plants. We show that these effects may arise from gibberellin (GA)-signaling defects. The signaling pathway of bioactive GAs depends on the proteolysis of their repressors, DELLA proteins. The repressor GA (RGA) DELLA protein represses plant growth, inflorescence, and flower and seed development. Our molecular data indicate that GCN5 is required for the activation and H3K14 acetylation of genes involved in the late stages of GA biosynthesis and catabolism. We studied the genetic interaction of the RGA and GCN5; the RGA can partially suppress GCN5 action during the whole plant life cycle. The reduced elongation of the stamen filament of gcn5–6 mutants is reversed in the rga–t2;gcn5–6 double mutants. RGAs suppress the GCN5 effect on the gene expression and histone acetylation of GA catabolism and GA signaling. Interestingly, the RGA and RGL2 do not suppress ADA2b function, suggesting that ADA2b acts downstream of GA signaling and is distinct from GCN5 activity. In conclusion, we propose that the action of GCN5 on stamen elongation is partially mediated by RGA and GA signaling.

Iaith wreiddiolSaesneg
Rhif yr erthygl6757
CyfnodolynInternational Journal of Molecular Sciences
Cyfrol25
Rhif cyhoeddi12
Dyddiad ar-lein cynnar19 Meh 2024
Dynodwyr Gwrthrych Digidol (DOIs)
StatwsCyhoeddwyd - 19 Meh 2024

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