Jack Szostak

Szostak, along with Elizabeth Blackburn, discovered that it was in fact a unique, repeating DNA sequence in the telomeres that protects the chromosomes from degradation — shortening because the lagging DNA strand has a gap at the end that can’t be filled — during replication. The sequence works by attracting and binding proteins that form a cap around the end of the DNA.

“The implications that the whole machinery was conserved across kingdoms; that was obvious as soon as we saw that the tetrahymena telomeres worked in yeast,” Szostak said of the discovery in an interview with Nobelprize.org. “And, basically I could see that it had worked as soon as I saw the results on the jelly. You could tell that we had linear plasmids in yeast and, therefore, that the telomeres were working. So, it was quite an exciting moment.”

The research is significant because damaged or shortened telomeres lead to premature cellular aging — and contribute to the aging of the entire organism. Subsequent research that built on Szostak’s work discovered that the enzyme telomerase is responsible for the cell’s ability to copy the entire length of DNA without missing the lagging portion. Continued study in this area has shed light on the relationship between aging and telomere shortening — and on cancer cells, which have the ability to divide infinitely with no telomere shortening. In both cases, researchers hope to be able to make clinical progress based on Szostak’s work.

Szostak’s current research focuses on the origins of life through the development of a synthetic cellular system capable of Darwinian evolution. His lab is also investigating model systems that may provide a route to artificial life with a biochemistry that is distinct from that of existing biology. Szostak is a professor of chemistry at the University of Chicago.