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Some physiological alteration associated with pleiotropic cross resistance and collateral sensitivity in
Abstract:
A mutant strain (2-20) isolated by growth on medium containing oligomycin and cycloheximide was also found to be cross resistant to antimyicn, cerulenin, chloramphenicol, tetracycline, triethyltin and triphenylmethylphosphonium bromide, but collaterally sensitive to dequalinium chloride, gentamycin, neomycin, paromomycin and thiolutin. Growth of 2-20, compared to the parental strain and 2 complete revertants, under a variety of environmental conditions revealed that strain 2-20 had an enhanced sensitivity to increased osmolality, elevated pH, and high temperature; in addition, strain 2-20 was unable to polymerize aminoimidazole ribotide at 37 degrees C as shown by the failure to develop a red colony in the presence of ade 2. Four complex solid media (glucose--KCI, galactose, ethanol, ethanol--KCI, Table 1) unable to sustain the growth of strain 2-20 were arbitrarily chosen to monitor cellular growth under different physiological conditions. Tetrad analysis indicated that the complex phenotype (cross resistance, collateral sensitivity, inablity to polymerize aminoimidazole ribotide, absence of growth under adverse physiological conditions) was inherited by an allele of a locus previously shown to result in a permeability barrier of the plasma membrane to chloramphenicol. 582 of 640 subclones used to isolate revertants of 2-20, under four different physiological conditions, were observed to produce a complete revertant of the complex phenotype. It is proposed that the pleiotropic phenotype could result from an alteration of the plasma membrane and mitochondrial inner membrane by a single nuclear gene mutation.
Insights
A yeast mutant exhibits complex drug resistance and sensitivity, alongside environmental sensitivities and impaired aminoimidazole ribotide polymerization. This pleiotropic phenotype likely stems from a single nuclear gene mutation affecting membrane permeability.
Area of Science:
- * Molecular biology and yeast genetics.
- * Cellular membrane function and drug resistance mechanisms.
Background:
- * A specific yeast mutant (2-20) was isolated exhibiting unusual growth characteristics.
- * Previous research linked a similar phenotype to plasma membrane permeability issues.
Purpose of the Study:
- * To characterize the complex phenotype of the 2-20 yeast mutant.
- * To investigate the genetic basis and potential cellular targets of this mutation.
Main Methods:
- * Phenotypic analysis of the mutant under various environmental and chemical stress conditions.
- * Genetic analysis using tetrads and subclone analysis to track inheritance of the phenotype.
- * Assessment of aminoimidazole ribotide polymerization capability.
Main Results:
- * The mutant displayed cross-resistance to multiple drugs and collateral sensitivity to others.
- * Enhanced sensitivity to osmotic pressure, pH, and temperature was observed.
- * Inability to polymerize aminoimidazole ribotide at 37°C was confirmed.
- * The complex phenotype was inherited as a single allele, linked to a known permeability locus.
Conclusions:
- * A single nuclear gene mutation likely causes the observed pleiotropic effects.
- * The mutation is proposed to alter both the plasma membrane and mitochondrial inner membrane.
- * This study provides insights into membrane function and drug resistance in yeast.