Arabidopsis BET bromodomain factor GTE4 regulates the mitotic cell cycle

• Published in: Plant signaling & behavior 2010-06, Vol.5 (6), p.677-680
• Main Authors: Della Rovere, Federica, Airoldi, Chiara A, Falasca, Giuseppina, Ghiani, Alessandra, Fattorini, Laura, Citterio, Sandra, Kater, Martin, Altamura, Maria Maddalena
• Format: Article
• Language: English
• Subjects: Addendum; animals; Arabidopsis; Binding; Biology; Bioscience; Calcium; Cancer; Cell; cell differentiation; cell proliferation; chromatin; Cycle; cytokinesis; gene expression regulation; genes; Landes; leaves; meristems; mitosis; mutants; Organogenesis; Proteins; seed germination; seeds; stem cells
• ISSN: 1559-2324; 1559-2316; 1559-2324
• DOI: 10.4161/psb.5.6.11571

Proteins containing bromodomains are capable of binding to acetylated histone tails and have a role in recognizing and deciphering acetylated chromatin. Plant BET proteins contain one bromodomain. Twelve BET-encoding genes have been identified in the Arabidopsis genome. Two of these genes have been functionally characterized, one shows a role in seed germination, the other is involved in the establishment of leaf shape. Recently, we characterized a third AtBET gene, named GTE4. We demonstrated that GTE4 is involved in the activation and maintenance of cell division in the meristems and by this controls cell numbers in differentiated organs. Moreover, the quiescent center (QC) identity is partially lost in the apex of the primary root of gte4 mutant, and there is a premature switch from mitosis to endocycling. Genes involved in the retinoblastoma (RB)-E2F pathway, which is important for coupling cell division and cell differentiation in plants and animals, were either up- or down-regulated in the gte4 mutant. In this report we also show that the defect in germination observed in gte4 mutant seeds is not rescued by the action of GA3. Further the root pole of the mutant embryo shows irregular cytokinesis in the procambial stem cells, and the QC of the lateral root shows a partial, but not transient, loss of QC identity. These additional results reinforce the importance of GTE4 in the control of cell proliferation.