Fundamental and applied research in ABA signaling: Regulation by ABA of the chromatin remodeling ATPase BRAHMA and biotechnological use of the PP2CA promoter.
- Autores: Marta Peirats Llobet
- Directores de la Tesis: Pedro Luís Rodríguez Egea (dir. tes.), Ramón Serrano Salom (tut. tes.)
- Lectura: En la Universitat Politècnica de València ( España ) en 2017
- Idioma: español
- Tribunal Calificador de la Tesis: José Antonio Jarillo Quiroga (presid.), Alejandro R. Ferrando Monleon (secret.), Laszlo Szabados (voc.)
- Programa de doctorado: Programa Oficial de Doctorado en Biotecnología
- Materias:
- Enlaces
- Tesis en acceso abierto en: RiuNet
- Resumen
Optimal response to drought is critical for plant survival and will affect biodiversity and crop performance during climate change. Mitotically heritable epigenetic and dynamic chromatin state changes have been implicated in the plant response to the drought stress hormone abscisic acid (ABA). The Arabidopsis SWI/SNF chromatin-remodeling ATPase BRAHMA (BRM) modulates response to ABA by preventing premature activation of stress response pathways during germination. Here, we show that the core ABA signalosome formed by ABA receptors, PP2Cs and SnRK2s physically interact with BRM to regulate BRM activity and post-translationally modify BRM by phosphorylation/dephosphorylation. Genetic evidence suggests that BRM acts downstream of SnRK2.2/2.3 kinases and biochemical studies identified evolutionary conserved SnRK2 phosphorylation sites in the C-terminal region of BRM. Our data suggest that SnRK2-dependent phosphorylation of BRM leads to its inhibition, and PP2CA-mediated dephosphorylation of BRM restores the ability of BRM to repress ABA response.
ABA plays a key role to regulate germination and post-germination growth and the AP2-type ABI4 and bZIP-type ABI5 transcription factors (TFs) are required for ABA-mediated inhibition of post-germination growth when the embryo encounters water stress. The growth arrest induced by ABI4 and ABI5 involves ABA signaling and in the case of ABI5, it has been demonstrated that ABA inhibits the activity of BRM to induce ABI5 transcription. Loss of BRM activity leads to destabilization of a nucleosome involved in repression of ABI5 transcription. Therefore reduction of BRM activity in the brm-3 allele leads to enhanced expression of ABI5 in 2-d-old seedlings and enhanced sensitivity to ABA. Novel genetic evidence obtained in this work indicates that ABI4 is one of the redundant TFs regulated by BRM that mediate ABA response during germination and early seedling growth. Thus, the association of BRM with the ABI4 locus together with the observed derepression of ABI4 expression in brm-3 suggests that BRM directly regulates ABI4 expression.
Finally, this work provides a direct link between the ABA signalosome and the chromatin-remodeling ATPase BRM, which enables ABA-dependent modulation of BRM activity as a possible mechanism to enhance plant drought tolerance. Additionally, we identified and characterized the promoter of PP2CA as a stress-inducible promoter and we have used it to drive the expression of ABA receptors from Arabidopsis and Solanum lycopersicum. This technology appears to be promising for the expression of ABA receptors in an inducible manner and to generate drought tolerant plants.
