## Abstract The rate of NAD turnover in microplasmodia of __Physarum polycephalum__ was investigated using a double labeling technique with (^14^C)‐adenine or adenosine and (^3^H)‐nicotinamide. The half‐life of an NAD molecule in __Physarum__ was estimated to be 25 min, which is shorter than in ei
Adaptation to trichodermin and anisomycin in Physarum polycephalum
✍ Scribed by Jessica A. Gorman
- Publisher
- John Wiley and Sons
- Year
- 1977
- Tongue
- English
- Weight
- 731 KB
- Volume
- 92
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The effects of the protein synthesis inhibitors trichodermin and anisomycin on the growth of the eucaryotic myxomycete Physarum polycephalum have been examined. When either of these drugs is added to log phase monoxenic cultures of myxamoebae, cell division is immediately arrested, but on continued incubation, growth resumes at a rate only slightly lower than that of drug free cultures. The length of the drug induced growth lag is roughly proportional to drug concentration. When adapted cells are transferred to fresh drug containing medium, growth is not inhibited. However, if the drug concentration is increased, transient inhibition is again exhibited. Measurement of the antibiotic concentration in used media demonstrates no significant external inactivation of either drug during adaptation. The resumption of growth cannot be attributed to the selection of stable drug‐resistant mutants: single amoebal colonies arising on drug plates are found to be as drug‐sensitive as control colonies when retested after subculture. In addition, when adapted cells are transferred to drug free medium, the phenotypic drug‐resistance is completely lost after several generations of growth. As recovery occurs in the continuous presence of drug and is not due to the accumulation of drug‐resistant mutants, this response appears to be an example of drug adaptation. Cross adaptation between anisomycin and trichodermin is also demonstrated, suggesting a common system is involved in adaptation to these structurally dissimilar, but functionally similar, drugs.
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