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Dr. Cameron Howard Lee, a postdoctoral fellow in the laboratory of Dr. Sue Biggins at Fred Hutchinson Cancer Research Center, has been named a 2019 Helen Hay Whitney fellow by the Helen Hay Whitney Foundation. The foundation provides independent postdoctoral research support to young biomedical scientists. Lee will use the three-year, $180,000 fellowship to investigate the potential relationship between protein production machinery and a cellular checkpoint that prevents abnormal separation of chromosomes during cell division.
“My project is going to be fleshing out this interaction, determining how functional it is, whether or not it’s a new paradigm for regulating this checkpoint,” Lee said.
“It’s great to have Cameron pursuing this project,” said Biggins, associate director of the Basic Sciences Division at Fred Hutch and a Howard Hughes Medical Institute investigator. “He developed the proposal himself and it’s exciting that the Whitney decided to fund it and recognize both his past contributions as a grad student and potential to be an outstanding postdoc. I am looking forward to mentoring him and supporting his postdoctoral work.”
Lee’s work focuses on a checkpoint that ensures dividing cells correctly portion out their chromosomes. When a cell undergoes division, it first replicates each chromosome —the long DNA strings in which our genetic information is stored — before parceling them out to both daughter cells. Each daughter cell needs exactly one copy of every chromosome. One too few or too many can impair proper cellular function and aneuploidy — the state of having the wrong number of chromosomes — is a hallmark of cancer.
Central to chromosome segregation is an enormous, multi-molecular machine called the kinetochore. The kinetochore, which attaches to each chromosome pair, provides the foundation to which microtubules, the protein ropes that pull chromosomes apart during division, attach. The cell senses when these microtubule-kinetochore attachments are properly made and allows chromosome segregation to proceed.
“What can happen and does happen in real life is that these attachments aren’t properly made,” Lee explained. “When they’re incorrectly made, there’s a surveillance system that detects that and signals to the cell, ‘Do not divide until we have everything attached and ready to go.’”
This “don’t go” signal is a critical cell-cycle checkpoint that is tightly regulated. Recent work in Biggins’ lab and elsewhere suggests that translation, the process by which proteins are produced, may be involved in this regulation and the transition from “don’t go” to “go.”
Lee wants to understand if and how translation is involved in this checkpoint and its interaction with the kinetochore-microtubule attachment surveillance system.
Ultimately, Lee aims to “flesh out the mechanism by which these [checkpoint] proteins are regulating translation or translation is regulating the checkpoint.”
