Mentorship for Transfer Student Success in STEM Research: Mentor Approaches and Reflections.

Mentorship has been widely recognized as an effective means to promote student learning and engagement in undergraduate research experiences. However, little work exists for understanding different mentors' perceived approaches to mentorship, including mentorship of students from backgrounds and educational trajectories not well represented in science, technology, engineering, and mathematics (STEM). Transfer students, in particular, face unique trajectories in their pursuit of research opportunities, yet few studies investigate how mentors describe their approaches to supporting these students. Using semistructured interviews, this study examines how mentors approach mentoring students from diverse backgrounds as research trainees, with an emphasis on transfer students. First, using phenomenography as an analytical approach, we identified four categories describing variations in how mentors reflected upon or accounted for the transfer student identity in their approaches. We find that research mentors vary in their understanding and exposure to the transfer student identity and may have preconceived notions of the transfer student experience. Second, we present vignettes to illustrate how mentors' approaches to the transfer student identity may relate or diverge from their general approaches to mentoring students from different backgrounds and identities. The emerging findings have implications for developing effective mentorship strategies and training mentors to support transfer students.

ChREBP is activated by reductive stress and mediates GCKR-associated metabolic traits.

Common genetic variants in glucokinase regulator (GCKR), which encodes GKRP, a regulator of hepatic glucokinase (GCK), influence multiple metabolic traits in genome-wide association studies (GWASs), making GCKR one of the most pleiotropic GWAS loci in the genome. It is unclear why. Prior work has demonstrated that GCKR influences the hepatic cytosolic NADH/NAD+ ratio, also referred to as reductive stress. Here, we demonstrate that reductive stress is sufficient to activate the transcription factor ChREBP and necessary for its activation by the GKRP-GCK interaction, glucose, and ethanol. We show that hepatic reductive stress induces GCKR GWAS traits such as increased hepatic fat, circulating FGF21, and circulating acylglycerol species, which are also influenced by ChREBP. We define the transcriptional signature of hepatic reductive stress and show its upregulation in fatty liver disease and downregulation after bariatric surgery in humans. These findings highlight how a GCKR-reductive stress-ChREBP axis influences multiple human metabolic traits.