MICHAEL WINOKUR PHOTOGRAPHYn late summer of 2005, budding developmental biologist Jeremy Reiter was expecting the three other members of his two-year-old lab for a celebratory dinner at his house. After weeks of working feverishly, they had finally resubmitted a revised manuscript to Nature. The paper told the story of how primary cilia—microtubular structures that jut out of cells’ membranes like antennae and help cells receive and interpret signals from the extracellular environment—were intimately involved in embryonic development, serving as the focal point for key components of the Hedgehog signaling machinery. Although these nonmotile cilia had been observed in the majority of vertebrate cells for more than a century, their function remained mostly a mystery. Reiter and his team had a feeling they had stumbled upon an important discovery.
But his excitement was short-lived. When his guests arrived, they served him with a paper that had just been published in Science, which told the exact same story. “It knocked the wind off my sails,” Reiter says. Having another team scoop his most promising project was very bad news for Reiter who was untenured and under a five-year research contract with the University of California, San Francisco (UCSF)—a temporary position he landed after his postdoc had been cut short when his mentor left for the UK.
METHOD: Luckily for Reiter, the paper was a hoax—a Photoshop creation courtesy of his lab mates. “Poor guy,” says conspirator and PhD student at the time Veena Singla between bursts of laughter, as she remembers how he snatched the impostor paper and ran to another room in panic. Today Reiter, who has since been the victim of many other pranks, laughs it off. A few weeks after that summer night, Nature accepted the paper1 and an offer for tenure at UCSF quickly followed.
RESULTS: Reiter’s passion for research was ignited during the PhD half of his MD/PhD training at UCSF, when he worked in Didier Stainier’s lab studying zebrafish heart and gut development. “Watching vertebrate development is such a beautiful process,” Reiter says. However, it was during his short-lived postdoc at UC, Berkeley that he became interested in cilia. Working with mice, he discovered a novel protein called tectonic which, when mutated, caused embryonic development to go haywire, disrupting both Hedgehog signaling and primary cilia formation.2 More recently his lab was the first to demonstrate that some human cancer cells are ciliated and that the cilium itself plays a role in tumorigenesis.3
DISCUSSION: Reiter’s PhD advisor Stainier describes him as fearless, creative, energetic, and terrific at training the younger generation of scientists. It was this enthusiasm that made Singla join Reiter’s lab as a first-year PhD student in 2003, despite how risky it was choosing a mentor who didn’t have a permanent position at UCSF. “It definitely worked out really well for me,” she says.
While Reiter continues to push the boundaries of what’s known about cilia’s role in health and disease, he is raising his two small children and becoming as proficient at playing the trombone as he is with the French horn.
- K.C. Corbit et al., “Vertebrate Smoothened functions at the primary cilium,” Nature, 437:1018-21, 2005. (Cited 281 times) Free F1000 Evaluation
- J.F. Reiter, W.C. Skarnes, “Tectonic, a novel regulator of the Hedgehog pathway required for both activation and inhibition,” Genes Dev, 20:22-27, 2006. (Cited 26 times)
- S.Y. Wong et al., “Primary cilia can both mediate and suppress Hedgehog pathway-dependent tumorigenesis,” Nat Med, 100:181-90, 2009. (Cited 34 times) Free F1000 Evaluation