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POSTERS: Biological control

Biological control of sudden decline syndrome of date palm caused by Fusarium solani using ACC deaminase producing actinobacteria in the UAE
Khaled Abbas El-Tarabily - United Arab Emirates University. Jawaher Haj Ali- United Arab Emirates University, Essam ElDin Saeed- United Arab Emirates University, Latifa Alnuaimi- United Arab Emirates University, Khawla Alwahshi- United Arab Emirates University, Aisha Alblooshi- United Arab Emirates University, Syn

Thirty three actinobacterial isolates were isolated from date palm rhizosphere in the United Arab Emirates (UAE). These were screened for their abilities to produce chitinase, ß-1,3-glucanase and antifungal metabolites active against Fusarium solani the causal agent of sudden decline syndrome (SDS) of date palm in the UAE. Only eight isolates showed in vitro exceptional antifungal metabolites and chitinolytic activity and caused the lysis of F. solani hyphae. These eight isolates were subsequently tested for their ability to produce 1-aminocyclopropane-1-carboxylic acid (ACC) deaminase, the immediate precursor of the stress hormone ethylene. Under greenhouse conditions, the ACC deaminase-producing (ACCD+) isolates were significantly more effective in reducing the incidence of SDS compared to ACC deaminase-non-producing (ACCD-) isolates. The application of these ACCD+ isolates resulted in the reduction of the in planta levels of ACC compared with date palm seedlings treated with the ACCD- isolates. The results clearly showed that ACCD+ isolates could replace Cidely® Top which is the currently recommended fungicide for the management of SDS of date palms in the UAE. The results showed the potential to enhance most, if not all, of the biocontrol agent’s performance by including the ACC deaminase ability into the biocontrol strains. This is the first study to demonstrate the superiority of antagonistic actinobacteria to enhance their effectiveness as biocontrol agents by their ability to produce ACC deaminase, antifungal metabolites and cell-wall degrading enzymes.