In memoriam: Roger A. Davis (1945-2008).

On Jun. 17, 2008, the lipid research community lost a beloved friend and scholar, Roger A. Davis. Roger was a major contributor to our understanding of the regulation of lipoprotein production, bile acid metabolism, and atherosclerosis. Roger gravitated to science at an early age; he loved to tinker and felt that the truthfulness of science provided a refuge from the conflicting religious orthodoxies between the two sides of his family. During his senior year of high school in Wilmington, Delaware, he befriended prominent DuPont chemist Howard Simmons, who taught Roger how to smoke cigars, drink scotch, and perhaps most importantly, love organic chemistry. Roger took to Simmons’ teachings, as he pursued chemistry for both his undergraduate and graduate degrees. After earning his doctorate in organic chemistry at Washington State University, he studied the biophysical aspects of bile acids in Fred Kern’s laboratory at the University of Colorado. But, it was in Dan Steinberg’s laboratory at UCSD where he first fell in love with biology and began what would become a lifelong involvement in the assembly and secretion of apolipoprotein B-containing lipoproteins. Throughout his career, Roger, who served on the faculties of Louisiana State University, University of Colorado, and San Diego State University, exuded an insatiable curiosity that led to his unusually broad view of important biological problems. Although he liked to refer to himself as a chemist working in biology, his interests encompassed diverse fields including nutrition, metabolism, immunology, and genetics, and he was not afraid to employ techniques from each of these areas. One of Roger’s most influential discoveries occurred in 1987 when he found that a substantial fraction of synthesized apoB was actually degraded somewhere along the secretory pathway. In fact, the amount of secreted apoB is determined by the amount rescued from degradation.1 In elegantly constructed and technically challenging experiments, Roger then demonstrated that critical segments of the apoB molecule require an interaction with microsomal triglyceride transfer protein (MTP) to be translocated across the ER membrane.2 He also demonstrated that apoB secretion was highly sensitive to MTP but not to free fatty acids or triglycerides.3 Of note, these significant findings preceded the appreciation of proteasomal and ER-associated degradation, now very active research fields in their own right. Roger was prescient in other areas as well; as early as 1983, he showed that, contrary to widespread scientific belief, bile acids do not exert direct feedback inhibition on bile acid synthesis.4,5 Subsequent discoveries would confirm his findings, clearly establishing that bile acids, through FXR, induce the intestinal expression of FGF 15 In Memoriam: Roger A. Davis (1945-2008)