Rate My Professor John David

John David is an Associate Professor of Biological Sciences at the University of Missouri-Columbia. He earned his PhD from Vanderbilt University in 1969. Over his extensive career at the university, he has held leadership positions, including Chair and Director of the Division of Biological Sciences. David has earned recognition for his contributions through several awards: President's University Citizenship Award for Service (2012), MU Honors College Faculty Excellence with Learning by Contract Award (2012), inaugural Mizzou Inclusive Excellence Award (2008), and Certificate of Appreciation of Leadership, Environmental Health & Safety (2005). He co-leads the Post-baccalaureate Research Education Program (PREP), housed in the Division of Biological Sciences, which offers individualized professional development and research training to underrepresented students to facilitate their transition to PhD programs in biomedical sciences. He has also served on advisory committees for the Ronald E. McNair Scholars Program.

The focus of Dr. David's research is the biochemical regulation of myoblast fusion during skeletal muscle development. His laboratory proposes that distinct stages of myogenesis involve specific cell surface protein receptors that transduce environmental signals and mediate cell-cell recognition, alignment, and fusion. Using a double immunization protocol against surface peptides present on normal myoblasts but absent on non-fusing variants, they generated monoclonal antibodies. Two such antibodies recognize developmentally regulated peptides that emerge shortly before fusion, concentrate at cell-cell contacts, and vanish post-fusion. Treatment with these monovalent antibodies inhibits fusion without impacting cell growth, attachment, or alignment. Paired with non-fusing myoblast variants, these tools enable molecular genetic dissection of fusion mechanisms. Further investigations into chick embryo skeletal myoblasts explored the roles of PGE1, cAMP, calcium influx from extracellular sources, calcium release from intracellular stores, and protein kinase C activation. Results delineate a signaling cascade: myoblasts release PGE1 in response to environmental cues, binding surface receptors to activate phospholipase C, liberate intracellular calcium and activate protein kinase C, trigger extracellular calcium influx initiating fusion. Concurrently, cAMP production promotes additional PGE1 release, propagating the paracrine signal across the culture.