These results lead us to propose a model for a mechanism for fast adaptations associated with the development of AFT: the effects of ethanol on a membrane protein, such as SLO-1, are countered by moving the protein into or out of specific membrane microdomains to achieve a more normal function of the neuron in the presence of ethanol. In this model, cholesterol and the TAGs on which LIPS-7 acts would constitute components of these microdomains that reduce the ethanol effect on the target protein, either by protecting the protein from ethanol or by changing the protein’s activity in opposition to the ethanol effect. An increase in the levels of these TAGs might lead to an increase in the size or quantity of these protective microdomains, thereby increasing the potential for minimizing ethanol’s effects on target proteins; decreases in the level of these TAGs would have the opposite effect on AFT. This model accounts for the altered rates and development of AFT in mutants for the ctbp-1, pag-3 and lips-7 genes, which regulate levels of these TAGs in different directions.
