Abutilon theophrasti is one of the global problematic weeds, which is resistant to the majority of common herbicides and allelochemicals. The seed coat of A.theophrasti is known to be inhabited by a number of microorganisms, including the zygomycete Actinomucor elegans. Based on previous observations, we hypothesize that A. elegans might be involved in the host's tolerance to the allelochemical benzoxazolinone (BOA). The results of A.elegans incubation with different concentration of BOA indicated the growth of A. elegans was unaffected by increasing concentrations of BOA in liquid culture and BOA was neither degraded by the fungus nor used as a carbon or nitrogen source. The fungus produced plant-growth-promoting compounds, like tryptophan, whose excretion was increased in the presence of BOA. With the intention of understanding the tolerance of A. elegans to BOA, membrane glycolipids and multidrug resistance transporters (MDR) inhibitors were studied. Inhibition of membrane multidrug resistance transporters by inhibitors had no effect on BOA accumulation by A.elegans, but the fungal growth and tryptophan excretion was inhibited. The fungal membrane lipids were extracted and analyzed by Thin Layer Chromatography (TLC), and identified as Sterol Glycoside (SG) and Glucosyl Ceramide (GlCer). The glycolipids were quantified by Quadrupole-time-of-flight (Q-TOF) Mass Spectrometer (MS) and the results indicated a higher GlCer accumulation rather than SG in the fungal membrane, also (Q-TOF) MS analysis of the fungal glycolipids, which was cultured in different nutritional deficiencies and toxicity levels revealed phosphorus deficiency and high concentration of BOA were effective stress in enhancing the GlCer accumulation.