Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros










Base de datos
Intervalo de año de publicación
1.
J Inorg Biochem ; 103(11): 1497-503, 2009 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-19740543

RESUMEN

In acid soils, aluminium (Al) toxicity and phosphate (Pi) deficiency are the most significant constraints on plant growth. Al inhibits cell growth and disrupts signal transduction processes, thus interfering with metabolism of phospholipase C (PLC), an enzyme involved in second messenger production in the cell. Using a Coffea arabica suspension cell model, we demonstrate that cell growth inhibition by Al toxicity is mitigated at a high Pi concentration. Aluminium-induced cell growth inhibition may be due to culture medium Pi deficiency, since Pi forms complexes with Al, reducing Pi availability to cells. Phosphate does not mitigate inhibition of PLC activity by Al toxicity. Other enzymes of the phosphoinositide signal transduction pathway were also evaluated. Aluminium disrupts production of second messengers such as inositol 1,4,5-trisphosphate (IP(3)) and phosphatidic acid (PA) by blocking PLC activity; however, phospholipase D (PLD) and diacylglycerol kinase (DGK) activities are stimulated by Al, a response probably aimed at counteracting Al effects on PA formation. Phosphate deprivation also induces PLC and DGK activity. These results suggest that Al-induced cell growth inhibition is not linked to PLC activity inhibition.


Asunto(s)
Aluminio/farmacología , Coffea/efectos de los fármacos , Fosfatos/farmacología , Transducción de Señal/efectos de los fármacos , Fosfolipasas de Tipo C/metabolismo , Aluminio/análisis , Células Cultivadas , Coffea/crecimiento & desarrollo , Coffea/metabolismo , Diacilglicerol Quinasa/efectos de los fármacos , Diacilglicerol Quinasa/metabolismo , Inositol 1,4,5-Trifosfato/antagonistas & inhibidores , Inositol 1,4,5-Trifosfato/metabolismo , Ácidos Fosfatidicos/antagonistas & inhibidores , Ácidos Fosfatidicos/metabolismo , Fosfolipasa D/efectos de los fármacos , Fosfolipasa D/metabolismo , Transducción de Señal/fisiología , Fosfolipasas de Tipo C/antagonistas & inhibidores
2.
J Inorg Biochem ; 102(8): 1631-7, 2008 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-18482769

RESUMEN

The primary Al-tolerance mechanism in plants involves exudation and/or accumulation of specific organic acid species, which form non-phytotoxic complexes with Al(3+) under physiological conditions. An evaluation was done of the role of organic acids in the tolerance mechanism of a cell suspension line of coffee Coffea arabica that exhibits Al-tolerance (LAMt) but for which the metabolic tolerance mechanism remains unknown. Significant differences existed in malate dehydrogenase and citrate synthase activities (key enzymes in organic acids metabolism) between protein extracts (day 7 of culture cycle) of the L2 (Al-sensitive) and LAMt (Al-tolerant) cells when cell suspensions were treated with 100 microM AlCl(3). HPLC analysis showed that the suspension cells of both lines exudate malate when incubated in a minimal solution but that exudation was not enhanced by treatment with AlCl(3) (100 microM). This is the first study demonstrating that plant Al-tolerance may be associated with down-regulation of malate dehydrogenase and citrate synthase activities.


Asunto(s)
Aluminio/farmacología , Ácidos Carboxílicos/metabolismo , Coffea/metabolismo , Tolerancia a Medicamentos , Citrato (si)-Sintasa/efectos de los fármacos , Coffea/citología , Coffea/efectos de los fármacos , Coffea/enzimología , Regulación hacia Abajo/efectos de los fármacos , Malato Deshidrogenasa/efectos de los fármacos , Malatos
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA