Related Experiment Videos
A cell membrane alteration specifically induced by SV40 transformation.
Journal of Cellular Physiology
|August 1, 1977
Summary
Simian virus 40 (SV40) transformation confers Amphotericin B resistance to cells by altering cell membranes. This specific genetic modification impacts sterol structure, offering insights into membrane function and antibiotic action.
Area of Science:
- Cell Biology
- Virology
- Molecular Biology
Background:
- Simian virus 40 (SV40) is a DNA tumor virus known to alter host cell properties.
- Lipophilic antibiotics like Amphotericin B target cell membranes, often interacting with sterols.
- Understanding virus-induced cellular changes is crucial for cell biology and therapeutic development.
Purpose of the Study:
- To investigate the effect of SV40 transformation on cellular resistance to Amphotericin B.
- To determine if this resistance is specific to SV40 and its underlying genetic control.
- To elucidate the membrane alterations responsible for Amphotericin B resistance.
Main Methods:
- SV40 transformation of mouse 3T3 and human fibroblast cells.
- Assessing cell viability and resistance to Amphotericin B.
- Investigating Amphotericin B binding to transformed and untransformed cells.
- Evaluating the effect of cholesterol supplementation on Amphotericin B resistance.
Main Results:
- SV40 transformation specifically induced resistance to Amphotericin B in both mouse and human cells.
- This resistance was not observed with polyoma or mouse sarcoma virus transformations, indicating SV40 specificity.
- Resistance was not due to reduced antibiotic binding and could be partially reversed by cholesterol.
- Results suggest a modification in membrane sterol structure or a loss of a critical cholesterol fraction.
Conclusions:
- SV40 transformation induces a specific, genetically controlled membrane alteration conferring Amphotericin B resistance.
- The mechanism involves changes in membrane sterol composition, likely affecting antibiotic interaction.
- This finding provides a model for studying virus-induced membrane changes and their functional consequences.