Likely Hydrolysis of Phoenix dactylifera Cell Wall Pectin by Fusarium oxysporum Pectin Methylesterase and Endo-polygalacturonase Activity Revealed in Vitro

Abstract

Fusarium oxysporum forma specialis albedinis is the causal agent of Phoenix dactylifera vascular fusariosis. It hydrolyzes the pectocellulosic wall of Phoenix dactylifera vascular tissue. Pectinases hydrolyze cell wall pectin, but they are not active in all strains, so it is not clear whether such hydrolysis is a mechanism of pathogenesis. This research tries to answer this question by testing the significance of pectin methylesterase and endo-polygalacturonase activity in hydrolyzing P. dactylifera cell wall pectin and suggests their mechanism of pathogenesis. Six F. oxysporum strains isolated from P. dactylifera of Beni Abbes and Ghardaia provinces were grown in glucose and in pectin, and the enzyme activity was measured with titrimetric methods. The activity in all strains was quantified and then compared with growth carbohydrates and provinces with statistical tests. We found that pectin methylesterase from both growth conditions hydrolyzed pectin, but endo-polygalacturonase was not active in glucose. Surprisingly, statistical tests showed that this inhibition was not caused by carbon catabolite repression. Pectin methylesterase was more active than endo-polygalacturonase in pectin and in strains isolated from P. dactylifera of Beni Abbes. We suggest that F. oxysporum inhibits endo-polygalacturonase, using an unknown mechanism. We conclude that the product of hydrolysis gradually blocks sap circulation and causes maceration of the rachis. We revealed that F. oxysporumhas a significant pectin methylesterase and endo-polygalacturonase activity, which can hydrolyze the cell wall pectin of P. dactylifera. Themaceration of date palms may be caused by these enzymes, and endo-polygalacturonase inhibition is not directly caused by glucose.