James Priess grew up in Wichita, Kansas. His father advertised farm machinery, and his mother took charge of raising the six children. From an early age Priess was fascinated by the abundance and diversity of life in neighborhood creeks and ponds, and was particularly amazed by frog development. He double-majored in biology and chemistry at Wichita State University, then decided to go to graduate school at the University of Colorado, Boulder. He planned to eventually teach biology at the high school or college level. “When I started I never thought of research as a career, and I didn’t even know what a postdoc was,” Priess says. “I thought you went to school to teach”. However, after working in various labs Priess changed his mind. “That was when I found that I really enjoyed doing research, and found it more interesting than teaching”. He was attracted to the nematode Caenorhabditis elegans as a model system partly because of its genetics, short lifespan, and small numbers of cells, but also because he discovered he was acutely allergic to the mice studied in a mouse embryology lab.
After receiving his PhD for studies on how the body shape of C. elegans was specified, Priess accepted a postdoctoral fellowship at the Medical Research Council (MRC) Laboratory of Molecular Biology in Cambridge, England. While there, Priess conducted an experiment that caused scientists to completely rethink how the early development of C. elegans compared with other organisms. The defining characteristic of C. elegans embryogenesis was thought to be a hard-wiring of early embryonic cells, such that each cell was intrinsically different from its neighbors. Instead, Priess demonstrated that he could swap the positions of certain early cells without disrupting development. This study and his later genetic studies showed that cell interactions had a fundamental role in early C. elegans development, as in higher organisms.
To understand the molecular basis for cell fate specification, Priess developed an innovative screening technique to identify maternally-provided genes that were critical for early development. He conducted these studies as a postdoc, and as faculty in his own laboratory at the Fred Hutchinson Cancer Research Center in Seattle, Washington. These screens led to a series of breakthrough studies by Priess and his collaborators. Among the identified genes are the PAR (partitioning) proteins that polarize the newly fertilized egg into distinct anterior and posterior regions. Other genes such as the transcription factor SKN-1 direct muscle development, while the PIE-1 gene keeps precursor cells that form the totipotent germline from responding to factors such as SKN-1. Additional diversification between somatic cells occurs through the POP-1 gene, which creates a remarkable binary system for specifying cell fates.
In subsequent work Priess studied diverse aspects of C. elegans genetics and cell biology, including studies on nematode viruses, morphogenesis (how tissues are shaped), and apoptosis (programmed cell death). Recently, Priess has used the nematode model to study how and why fat deposits (lipid droplets) occur inside the nuclei of some cells, including human cells. “We found that these droplets appear deleterious to intestinal cells, but not to germ cells, and have some hints about the basis for this difference” says Priess. This research may lead to a better understanding of the impact that body fat has on our bodies and our health.
Priess has received many awards and honors for his work over the years, including membership in the National Academy of Sciences. He has also been an investigator of the Howard Hughes Medical Institute (1999-2011). Priess lives in Seattle with his wife, June. When not in the lab, Priess enjoys drawing and reading history.