Elizabeth H. Blackburn


Nobel Prize Talks: Elizabeth Blackburn

Released 2014-03-27

People age biologically at very different rates, according to Elizabeth Blackburn. In this conversation the 2009 Nobel Laureate in Physiology or Medicine discusses how her scientific discoveries concerning telomeres transform the way we look upon aging, and as longevity increases over time, how we can look upon the elderly as a resource. She also encourages us to open our eyes to the beauty of nature, and explains why working with a mixture of people from diverse backgrounds is one key to scientific and creative success.

Play 49 min.

Interview, December 2009

Interview with the 2009 Nobel Laureates in Physiology or Medicine Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak, 6 December 2009. The interviewer is Adam Smith, Editor-in-Chief of Nobelprize.org.

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Nobel Minds 2009

The 2009 Nobel Laureates met at the Bernadotte Library in Stockholm on 9 December 2009 for the traditional round-table discussion and TV program ‘Nobel Minds’. The Laureates discussed the controversy surrounding President Barack Obama’s Nobel Peace Prize, climate change data and science’s integrity in the face of political policy.

Participants of the 2009 edition of Nobel Minds were the Nobel Laureates in Physics Willard S. Boyle and George E. Smith; the Nobel Laureates in Chemistry Venkatraman Ramakrishnan, Thomas A. Stetz and Ada E. Yonath; the Nobel Laureates in Physiology or Medicine Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak; the Laureates in Economic Sciences Elinor Ostrom and Oliver E. Williamson. Program host: Zeinab Badawi.

Telephone interview with Elizabeth H. Blackburn immediately following the announcement of the 2009 Nobel Prize in Physiology or Medicine, 5 October 2009. The interviewer is Adam Smith, Editor-in-Chief of Nobelprize.org.

Interview transcript

[Elizabeth Blackburn] Hello.

[Adam Smith] Good morning, may I speak to Elizabeth Blackburn please?

[EB] This is she speaking.

[AS] Hello, it’s Adam Smith, calling from the Nobel Foundation web site.

[EB] Oh, yes. I was told to expect your call.

[AS] How nice. Thank you and congratulations.

[EB] Thank you.

[AS] It’s terrifically early in the morning where you are, I guess?

[EB] Don’t even tell me how early it is!

[AS] Had you managed to go to bed before they woke you up with the call?

[EB] Well, I had, yes. But, the night was definitely truncated – in a good way.

[AS] Indeed. I’ve just spoken to Carol Greider and Jack Szostak and to them I asked the same thing: you presumably had a suspicion that this was on the way, given the number of prizes that have been coming your way recently?

[EB] Well, there had been some press speculation which I had tried to ignore. But, believe me, it still was a very great surprise.

[AS] Now, the Prize has been awarded for research work you did mainly during the early 80s …

[EB] Right, right.

[AS] But, you’ve devoted your whole life to telomeres and I wanted to ask what was their particular fascination for you?

[EB] Well, so many aspects. First of all, just how does it work? Why are telomeres working the way they do? And, every time we looked with an experiment, we would find something ever more complicated and clever that the cell did. And, we realized the old truism from the original cytogenetics which was that the telomere is really important for protecting ends and, as you might expect, the cell actually devotes all sorts of machinery to make sure that never goes wrong, or goes wrong as little as possible. And so that intricacy, the machinery is really just a marvellous thing. And then in recent years it has become very interesting to look at what happens to telomeres in humans because they really do seem to reflect our status of health and our risk of disease in quite a striking way that suggests that what one sees at telomeres gets integrated from a lot of different inputs but it really serves as a kind of indicator of how well cells are doing. So it’s just been endlessly fascinating because the science of it is endlessly fascinating.

[AS] I want to turn to humans in a second. But, the original observations you just mentioned about the protective role of telomeres were made in the 30s by Muller and McClintock, for instance.

[EB] That’s right, absolutely. And, we always have to remember that they worked from the deduction of genetics and cytogenetics with no knowledge that even the genetic material was DNA. And so, what my work had been doing was to first of all show the molecular nature of the telomeric DNA itself and then with Jack Szostak we were able to extend that and show that something strange was going on. And, then with Carol, that was when we worked together to hunt for this enzyme, or activity that we suspected existed, which was telomerase. So that put these cytogenetic observations onto a molecular footing. You know, before the telomere had sort of been the ‘blob’ at the end of the chromosome.

[AS] Exactly. It had sort of lain there for decades, if you like. Known about, thought about, but nobody was particularly able to tease apart its function.

[EB] Right. Like so many things in science, it depended on first of all understanding what was the nature of the chromosome, which was DNA as well as proteins. And, then, thinking about, as Kornberg did, thinking about how DNA is replicated – not only thinking, he showed – and then that showed that there were problems with replication at the ends of chromosomes. And so that was one of the big impetuses for looking for telomerase, which was to try to see how the cells answer the question of how their incomplete replication problem gets solved.

[AS] In your sort of journey through telomeres, how much has been dependent on finding the right companions to work with? Because, for instance, you met Jack Szostak at a Gordon conference in 1980. Or, at least, you decided to collaborate then.

[EB] Right, right. I think that’s the way all science happens, right. And, I suppose there’s an element of chance favors the prepared mind. But, that’s the way science happens. It’s a lot of meetings of minds and the concepts of telomeric DNA and the sequencing, well that was very dependent on the sequencing methodologies that were being worked out even before the now conventional methods of DNA sequencing happened. We didn’t use those. I was using very unconventional methods to sequence the telemetric DNA originally. Methods devised by, for example, my husband John Sedat and Ed Ziff while we were in Cambridge in England.

[AS] That’s right. Because you were post docs together with Fred Sanger, is that …

[EB] I was a graduate student with Fred Sanger and John Sedat, who is now my husband, now, he was a post doc. So, everything builds on other technologies so I was building on … I was curious about the ends of chromosomes and building on technologies, completely, which were methods of sequencing DNA and people like Ray Wu and Murrays in Edinburgh, all these people had been figuring out ways to sequence the very ends of chromosomes. So, it’s a tremendous sort of interactive process, as I’m sure you have heard a thousand times!

[AS] But, it’s nice to hear it described. Your current work is, as you said, fixed on humans and in particular on the relationship between chronic stress and telomerase …

[EB] Yes, we’re very interested in that. That’s a corner of my lab. You know, we have part of our lab where we interact with clinical colleagues and one in particular at my institution, Elissa Epel, who was the person who first started to ask with us this question of chronic stress and how was it related to telomere maintenance? Actually, we still do a lot of basic research. We’re still fascinated by those same questions you addressed earlier. You know, what is it that keeps you so interested in the telomere? It’s so intricate and complicated and you want to know how it works. Actually, most of my lab does the very basic research. The chronic stress part, is to me, just fascinating though. Because it is really related to what a lot of humanity undergoes.

[AS] And, is it the case that telomere length and maintenance is affected directly by stress and is that, perhaps, causative of problems that then arise from stress? Or is it some kind of epiphenomenon?

[EB] There’s two parts to the question. So, one is, the association of telomere shortness, and actually even poorly regulated telomerase we’re finding, that association and chronic stress is very real. And, there are certain situations where our studies – and Elissa Epel has looked at cohorts of women who are caregivers of a chronically ill child, and more recently even dementia caregivers, where the dementia patient is their husband or partner – what we find is that it really does look causative. Particularly, in one study, the number of years that a mother had been in her situation was related to the extra telomere shortness and the dampening of telomerase. And, that made us really think that this is likely to be causative. Because, number of years relating to those parameters, it’s very – number of years the person was in that stressful situation relating to those parameters being worse – it’s very hard to imagine a scenario where it could work the other way round. That the shortness of the telomeres and the dampened telomerase was causing that mother to have been in that situation, one year, five years, twelve years, it doesn’t logically follow. So that kind of evidence makes us think that there is a causality. Now, the question is, does that cause the bad, clinical effects of stress, which have been well-documented in the literature for years and years. Does the telomere shortening cause it? It’s a plausible model actually. And, I’m inclined to think it does. But, you have to be very careful about what exactly is the complete mechanism by which these adverse effects of stress are mediated. But certainly we see the effects on telomere maintenance in the immune system which is, it turns out, a very good window into what’s happening in terms of disease risks in the body. So we do think that there’s a lot of good reason to think that it might actually be a causative chain.

[AS] Your window into the immune system in that case is studying white blood cells. Is that correct?

[EB] That’s the one that participants in studies give you and we now look at many, many different cohorts of various kinds. And, generally, we try to have a situation where the person is healthy so you’re not confounded by disease. So, that means that healthy individuals are donating their blood samples for the studies. So, blood is one of the cell types one can look at.

[AS] I just wanted to ask you one last thing which was that it’s been commented previously that telomerase and telomere research is a field which has, happily, a large number of women working in it. Do you agree with that and is that something that …

[EB] Yes, and, I’ll turn your comment around and say it’s fairly close to the biological ratio of men and women. It’s all the other fields that are aberrant.

[AS] Absolutely, yes.

[EB] This is the normal field, right? Because it is a much more even distribution between men and women, absolutely. No, I can’t compare with other fields. You know, this is the one I know. But, it is true.

[AS] Yes, but is it something you think you have actively worked on promoting, to make it like that?

[EB] You know, I’ve only actively promoted what we always hope is good science. And, then it’s not as if one would favor a woman researcher in the area over a man researcher in the area. But, women have come into this field perhaps because in the molecular days of the field, that is the kind of things that I’ve been doing and that Carol … we were women, we tended to have women students and post docs, which was not 100%. They tended to be 50-50, men and women, which is already a little higher than the usual ratios. And so there’s a sort of self-perpetuating aspect to that. Because there’s nothing particularly about the science per se which has any, sort of gender-like quality to it. You know what I’m saying? I think we’re looking very much at sort of sociological phenomena here.

[AS] Yes, but one might hope that since it’s seen to be possible in this field it could be possible in all fields.

[EB] You really do hope that when people see something like this working, that this could be seen as, that this would be, the norm. And, the different ratios of men and women researchers in other fields would be the aberrancy. That’s what I’d like to see, because you want women to have access to science because it’s such a wonderful thing to do. Anything that makes it more feasible for women to be in science and do the science they like, that’s good.

[AS] Thank you, that’s a good note to stop on for now. Thank you very much for giving us your time. When you come to Stockholm in December, then happily we have the chance to interview you at greater length.

[EB] Great, and hopefully, I’ll be a little less sleepy!

[AS] Do you plan on trying to return to sleep tonight or is the day beginning?

[EB] Hmm. Well, I’ve made a couple of calls to the family and I might try and get a little sleep right now. That might be a good idea. It is after all three in the morning.

[AS] Good luck with it.

[EB] Nice to talk to you.

[AS] Thank you very much indeed, bye, bye.

[EB] Thank you, bye.

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To cite this section
MLA style: Elizabeth H. Blackburn – Interview. NobelPrize.org. Nobel Prize Outreach AB 2024. Tue. 16 Jul 2024. <https://www.nobelprize.org/prizes/medicine/2009/blackburn/interview/>

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