I photographed Elizabeth Blackburn at her home in San Francisco in 2023. In the stillness of her home, it was easy to settle into conversation. Her work concerns something happening constantly within us, beyond our awareness: how cells protect the ends of their chromosomes, and what happens when that protection begins to fail.

Each time a cell divides, it must copy its DNA. Yet the machinery doing the copying cannot fully reproduce the very ends of a chromosome. Without protection, genetic information would gradually be lost. Life depends on getting this small detail right, over and over again.

Blackburn’s interest in living things began in Tasmania. Born in Hobart to parents who were both physicians, she spent her early childhood in the seaside town of Snug, picking up ants in the backyard and jellyfish on the beach. Biology was something she could hold and examine long before it became a profession. Her studies took her to Cambridge, where she learned to sequence DNA in Frederick Sanger’s laboratory, and then to Yale to work with Joseph Gall.

There she studied Tetrahymena, a tiny freshwater organism. At the ends of its miniature chromosomes, she identified a short sequence of DNA repeated many times. These stretches belonged to the structures called telomeres. Working later with Jack Szostak, she helped demonstrate that the sequences could protect chromosome ends, even when transferred between different organisms. A pond organism and yeast shared a fundamental solution to the same problem.

But how were those repeated sequences made?

At Berkeley, Blackburn and her graduate student Carol Greider searched for an enzyme that could build them. On Christmas Day in 1984, Greider developed a film showing the first evidence of its activity. Further experiments established what they had found: telomerase, an enzyme capable of adding DNA to chromosome ends. In 2009, Blackburn shared the Nobel Prize in Physiology or Medicine with Greider and Szostak.

The implications reached into aging and cancer, though they resisted any simple promise of longer life. Many human cells lose telomeric DNA as they divide. When that protection becomes critically depleted, cells can stop dividing. Cancer cells, meanwhile, often use telomerase to sustain their growth.

Blackburn’s later work brought these molecular questions closer to ordinary human experience. With psychologist Elissa Epel and colleagues at UCSF, she investigated connections between chronic stress and telomere biology. Their 2004 study of mothers, including women caring for chronically ill children, found an association between greater perceived stress and shorter telomeres in immune cells. It raised questions about how the circumstances of a life might reach into its cells, although an association alone could not establish cause.

I enjoyed the ease of being with her. The conversation had room for uncertainty, which seems essential when the subject is life itself. Her discoveries had answered questions that once appeared almost inaccessible, then opened others with consequences far beyond the laboratory.

What draws me to Blackburn’s story is where it began: someone looking closely at a small organism, following a repeating pattern at the end of a strand of DNA. There was no way to see all that would follow. First, there was something she wanted to understand.