The Nobel Prize Medal (from nobelprize.org)

The University hasn’t directly won any of the first two Nobel Prizes awarded this week, but one of today’s winners has a UChicago connection: George E. Smith, one of three scientists who will share the $1.4 million prize in physics, received his doctorate at the University of Chicago 50 years ago in 1959. And Monday’s prize has a much more tenuous connection to the proprietor of this very blog, which I’ll explain below.

First, today’s prize rewarded innovations that power technology integral to our daily lives: digital cameras and the Internet. Smith and Willard S. Boyle received the award for the invention of charge-coupled devices, CCDs, the technology put to work in the millions of digital cameras now in use. Charles K. Kao, the third recipient of today’s award, was responsible for improving the use of fiber optic cables, changing the material used in those cables to dramatically extend the distance that light can travel within. Thanks to Dr. Kao, I can quickly research this blog post and you can quickly read it, downloading the information through fiber optic cables that he helped create.

Monday, the award was given to three scientists who made crucial advances in the study of chromosomes, cancer and aging. No, it wasn’t Janet Rowley, but her friend Elizabeth Blackburn was one of the awardees alongside Jack Szostak and Carol Greider. The trio were honored for the discovery of telomeres, repeated sequences at the ends of DNA that prevent genetic material from being damaged and degraded every time a cell is replicated. There really is no better metaphor to explain the function of telomeres than the one used by the Associated Press all day yesterday: “It’s been compared to the way plastic tips on the ends of shoelaces keep the laces from fraying.”

In honor of their award, Scientific American republished an excellent article by Greider and Blackburn that explains why telomeres (and their enzyme partner telomerase, which preserves telomere length) are significant to the study of aging and cancer. As people and their cells age, telomerase works less efficiently, and telomeres and chromosomes shrink, making the cell replication process less accurate. The inability to create new cells could lead to conditions associated with old age, such as artherosclerosis and a weakened immune system. In cancer cells, on the other hand, telomerase is a bad thing, allowing tumor cells to replicate rapidly, grow, and spread around the body. Researchers have thus turned to telomerase inhibitors as a potential cancer treatment.

It is with tongue firmly in cheek that I note my nanoscale contribution to the field of telomere research, from my time at the National Institute of Child Health and Human Development in 2002. I worked in the laboratory of Jeffrey Baron, who studied mechanisms of bone growth in children. As humans grow, a strip of cartilage in the bones of arms and legs called the growth plate produces new cells that lengthen those bones; some time after puberty, those growth plates disappear. With Ben Nwosu and Ola Nilsson, we studied whether the telomeres in those growth plates grow shorter with age - I mostly helped by doing dissections on our chosen animal model, the rabbit, as we bantered about World Cup results. Somewhat unfortunately, we found that the telomere length does not change as a rabbit grows older, suggesting that telomeres are not responsible for the closing of the growth plate after puberty. But disproving a hypothesis is just as important sometimes as proving one, and we were able to publish the results in the journal Hormone Research.

So on behalf of telomere researchers the world over, I’d like to thank the Nobel Committee for their award. But I’ll happily defer the prize money to Blackburn, Grieder and Szostak.

In each cell of the body is a busy factory, containing all of the elements needed for that cell to develop and perform its unique function. A neuron sprouts a long extension and develops the ability to conduct electrical impulses. A liver cell secretes bile and can absorb toxic substances to neutralize them. Muscle cells elongate, form multiple nuclei and build long fibers that contract powerfully when stimulated.

But as different as the end product may be, the machines that make up the inner workings of these cells are largely the same, built from the identical set of genetic instructions that all cells share. Indeed, all of the body’s hundreds of cell types originate from one ambitious type of cell with the potential to become almost anything – the pluripotent stem cell to which so much scientific attention has been recently paid. What destiny that neutral cell follows is largely determined by how it organizes its factory, placing its machines in various orders that can have dramatically different outcomes.

Charting those interactions in specialized cells is a frequent goal of scientific research, as understanding a cell’s inner workings will help doctors make repairs when something goes wrong. The laboratory of Dr. Marcus Clark, chief of the Section of Rheumatology at the University of Chicago Medical Center, has devoted itself to the machinery of the B cell, the immune system cells responsible for producing antibodies that fight off disease. In a paper published this week in the journal Nature Immunology, Clark’s group fills in much of the story of what signals are involved in a crucial step of early B cell development, and shows that one of those signals, called Ras and typically associated with cancer in other cells, is surprisingly a key component in the healthy formation of a B cell.

“Ras is one of the best described oncogenes out there, it contributes to cancer in a variety of different formats.” Clark said. “It’s always seen as this pro-proliferative thing: if you put Ras in, the cells start dividing autonomously, and that’s cancer. In our hands, Ras turned off proliferation, it was very unexpected.”

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Kenneth Miller gave a typically captivating talk at the AAAS meeting yesterday in which he showed an eye-popping video illustrating what goes on in our cells all the time.

Ken was kind enough to send us a link to the full library of videos, by the BioVisions group at Harvard University. Here’s a YouTube video with highlights - watch for the big vesicle being tugged along a microtubule by a motor protein with little protein “shoes.”