DIACYLGLYCEROL KINASE IOTA LINKS HEAT SHOCK GENE EXPRESSION TO THE SUPPRESSION O

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Disruptions in autophagy have been reported in several diseases, including neurodegeneration and some types of cancers. Despite being regulated by similar conditions, the interplay between heat shock and autophagy is unclear. The goals of this project are to examine the impact of the heat shock response on autophagy and the define the responsible signaling processes. Our preliminary findings identified the lipid kinase DGK as a potential cross-talk mediator. The product of DGK, phosphatidic acid (PA) inhibits autophagy through the mTOR protein kinase. The Specific Aims of our INBRE project are: 1. Evaluate the relationship between HSF1-dependent gene expression and autophagy; 2. Explore the regulation of DGK and PA levels by heat shock; and 3. Evaluate the relationship between DGK and autophagy.