Ganoderma boninense, the causative agent behind basal stem rot (BSR) disease in oil palm, instigated a pressing need for innovative and ecologically sustainable strategies to counter its impact. Biological control strategies, particularly employing bio-fungicides, have emerged as environmentally friendly alternatives for managing oil palm plant diseases. This study delved into harnessing the biocontrol potential of Indigenous bacterial isolate by investigating and evaluating its bioactive compounds of ethyl acetate extract with the capacity to suppress G. boninense growth in oil palm plants. Molecular identification was utilized to identify of bacterial isolate using 16S rRNA primers (5′- AGA GTT TGA TCC TGG CTC AG– 3′) and (5′- GGA TAC CTT GTT ACG ACT T– 3′). The agar well diffusion technique and scanning electron microscopy (SEM) were utilized to assess the inhibitory effects of bacterial ethyl acetate extract against G. boninense. A comprehensive analysis of the bacterial ethyl acetate extracts was conducted by gas chromatography - mass spectrometry (GC–MS). Molecular identification confirmed that the bacterial isolate was Bacterium strain BS1727. By employing SEM, the ethyl acetate extracts had influenced on G. boninense mycelial architecture. The exposure to the bacterial ethyl acetate extracts induced degradation and morphological distortion of the mycelial structure, serving as an indicator of its impact on the mycelium's structural modulation. Noteworthy, the spectrum of bioactive compounds was a subset of aromatic hydrocarbons, encompassing volatile organic compounds (VOCs). Based on GC–MS analysis, among the VOCs, acetic acid butyl ester and toluene showed the highest relative peak areas, 46.34 % for acetic acid butyl ester and 31.82 % for toluene, respectively. Ethylbenzene had a relative peak area of 5.4 %, 1,1,2-trichloroethane 4.41 %, and allyldimethyl (prop-1-ynyl) silane 3.17 %. The remaining compounds were 6-undecyl-5,6-dihydro-2H-pyran-2-one, 3-decen-5-one, 2-methyl-, and o-cymene, with the relative peak areas were below 1 %. These findings explained the inherent capacity of antifungal compounds as a viable strategy in inhibiting the growth of G. boninense.
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