IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Role for nitric oxide and reactive oxygen species in the induction of potassium transport during potassium deficiency.
Autor/es:
PERALTA, ML; MANGANO, S; MORICONI, JI; BUET, A; SIMONTACCHI, M; SANTA-MARÍA, GE
Lugar:
Buenos Aires
Reunión:
Workshop; Oxidative Stress and Antioxidants; 2009
Institución organizadora:
Facultad de Farmacia y Bioquímica-UBA, CONICET
Resumen:
The magnitude and properties of potassium (K+) uptake from the soil solution depend on the media encountered by roots during growth. The ionic environment controls the contribution of alkali cation transporters to K+ capture by affecting their activities as well as the accumulation of transcripts coding for them. In this work we explored the possibility that following K+ withdrawal the enhancement of K+ transport from diluted K+ solutions and the expression of genes coding for HAK and HKT transporters involved in the acquisition of alkali cations are related to the metabolism of nitric oxide (NO) and reactive oxygen species (ROS). Experiments conducted with one week old barley (Hordeum vulgare) plants revealed that a short-term exposure to K+-deprivation (6 h) leads to enhanced Rb+-uptake and enhanced accumulation of HvHAK1, HvHAK1b and HvHKT2;1 transcripts. Addition of the NADPH-Oxidase inhibitor DPI, the superoxide dismutating agent MnCl2, as well as the NO scavenger cPTIO, during the K+-deprivation period precluded Rb+-uptake enhancement. In turn, the presence of cPTIO avoids the enhanced accumulation of all the above mentioned transcripts. Interestingly, the effect exerted by DPI and MnCl2 on transcripts accumulation was clearly different for the almost identical genes HvHAK1 and HvHAK1b.  Our results indicate that ROS and NO are required for the appearance of the inducible component of K+ transport, and also that changes in the balance of ROS differentially affects the expression of alkali cation transporter-coding genes. Supported by CONICET and ANPCyT