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Trichodermin esterase activity and trichodermin resistance in Mucor racemosus
Antimicrobial Agents and Chemotherapy
|April 1, 1986
Summary
Mucor racemosus develops resistance to trichodermin by deacetylating the drug. This adaptation, triggered by trichodermin or cycloheximide exposure, involves rapid deacetylation, rendering the antibiotic less effective.
Area of Science:
- Biochemistry
- Mycology
- Molecular Biology
Background:
- Mucor racemosus is a fungus.
- Protein synthesis inhibitors like trichodermin are crucial in antifungal research.
- Understanding resistance mechanisms is vital for developing effective antifungal strategies.
Purpose of the Study:
- To investigate the mechanism of inducible phenotypic resistance in Mucor racemosus towards the protein synthesis inhibitor trichodermin.
- To elucidate the role of deacetylation in trichodermin resistance.
Main Methods:
- Exposure of Mucor racemosus to trichodermin and cycloheximide to induce resistance.
- Measuring the uptake of radiolabeled [14C]trichodermin in adapted and nonadapted cells.
- Assessing the deacetylation of trichodermin to trichodermol in vivo and in vitro.
Main Results:
- Mucor racemosus demonstrated inducible resistance to trichodermin after exposure to the drug or cycloheximide.
- Both adapted and nonadapted cells absorbed trichodermin, but adapted cells exhibited more rapid deacetylation to trichodermol.
- Trichodermol, the deacetylation product, was found to be a poor inhibitor of Mucor growth.
Conclusions:
- The primary mechanism of trichodermin resistance in Mucor racemosus is the deacylation of the active antibiotic.
- Rapid deacetylation of trichodermin by adapted cells effectively neutralizes the drug's inhibitory effect.
- This study highlights a key enzymatic detoxification pathway contributing to antifungal drug resistance.