The reduction of FM4-64 and Lucifer yellow uptake in the absence of Sac6 supports the idea that actin is still important for this endocytic pathway. The level of Lat-A added is likely to have an impact on F-actin stability, as it is known that low levels of the drug are remedial for cells with stabilized actin structures. It is not yet known whether these changes in stability impact on the subset of actin binding proteins that are able to interact with actin in these cells which in turn might affect the form of invagination that can be generated. A function for the amphiphysin Rvs167 in the Abp1-mediated pathway might provide a route for membrane curvature and possibly membrane scission. The yeast amphiphysins Rvs167 and Rvs161 are generally considered to function as an obligate dimer which can bind to phosphoinositol 4,5 bisphosphate containing Dabrafenib membranes and generate curvature and possibly participate in lipid phase separation which might in some cases be able to lead to scission. Another outcome from this work is the demonstration of the negative effects of tagging. Much work in yeast has been generated from such studies but it is increasingly clear that while a tag might not be detrimental for growth in normal lab conditions, such tags are likely to affect at least a subset of protein function. In this case, different tags caused distinct levels of inhibition in Abp1 function supporting the importance of data from other approaches in drawing conclusions. In summary, we have reported the existence of an Abp1mediated endocytic pathway in S.cerevisae. The pathway continues to function in the presence of low levels of the actin monomer binding drug Lat-A, though F-actin is required for pathway function. We propose that yeast cells maintain distinct but overlapping endocytic pathways to allow fluid and lipid uptake even when environmental conditions may alter their capacity for more cargo driven routes. Intracellular lipid accumulation, inflammatory responses, and apoptosis are the major pathogenic events of many metabolic disorders, including atherosclerosis and nonalcoholic fatty-liver diseases. Increasing evidence shows that nuclear receptors play critical roles in the regulation of lipid metabolism and inflammatory responses. Nuclear receptors are ligandactivated transcription factors that affect processes as diverse as reproduction, development, inflammation, and general metabolism through regulating target gene expression. Many nuclear receptors function as sensors of cellular cholesterol and lipid levels.