02079nam a2200217Ia 4500003001000000005001700010040000900027245012200036490006600158520124200224650002501466650002301491650001901514650002001533700002401553700002801577700002501605700003401630856015601664008004101820MX-MdCICY20260521091241.0  cCICY10aEffect of phosphate on aluminium-inhibited growth and signal transduction pathways in Coffea arabica suspension cells0 vJournal of Inorganic BioChemistry, 103(11), p.1497-1503, 20093 aIn 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 (IP3)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.14aPHOSPHATE DEFICIENCY14aALUMINIUM TOXICITY14aCOFFEA ARABICA14aPHOSPHOLIPASE C12aChee-González, L.12aMuñoz-Sánchez, J.A.12aRacagni-Di Palma, G.12aHernández-Sotomayor, S.M.T.40uhttps://drive.google.com/file/d/1qbsUUNlGsx4b6vtBqf3HdXKfaB4nZfEp/view?usp=drivesdkzPara ver el documento ingresa a Google con tu cuenta: @cicy.edu.mx250602s9999    xx |||||s2   |||| ||und|d