In Honor of Elizabeth Blackburn’s 75th Birthday: Celebrating the Discovery of Telomeres
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: 20 June 2024 | Viewed by 3018
Special Issue Editors
Interests: physiological consequences of DNA damage at the cellular and organismal level mainly in mammals; DNA damage response (DDR); DNA repair
Interests: oocyte aging; telomeres; mitochondria; DNA-methylation
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Special Issue Information
Dear Colleagues,
Elizabeth Blackburn was born on November 26th, 1948, in Hobart on the island of Tasmania, Australia. Both of her parents were doctors. Blackburn took an early interest in animals and nature and went on to study biochemistry at the university in Melbourne. She later received her Ph.D. from Cambridge University, England. Prof. Blackburn moved to Yale University in New Haven, USA, and later to the University of California in San Francisco, and she has taken an interest in the ethical implications of research and has contributed to the creation of a code regulating the field. Together with Carol W. Greider and Jack W. Szostak she received the Nobel Prize in Physiology or Medicine for "the discovery of how chromosomes are protected by telomeres and the enzyme telomerase" in 2009.
Telomeres are the genomic portions at the ends of linear chromosomes. Telomeric DNA in vertebrates is made of TTAGGG repeats bound by a set of proteins that modulate their biological functions and protect them from being recognized as DNA damage that triggers a DNA damage response (DDR). As standard DNA polymerases cannot fully replicate linear DNA templates in the absence of telomerase, a DNA-template-independent DNA polymerase, and because of nucleolytic processing, DNA replication results in the generation of chromosomes with progressively shortened telomeres. As telomeres reach a critical length, they become unable to bind enough telomere-capping proteins and are sensed as exposed DNA ends, which activates the DDR pathways that, through the induction of the cell cycle inhibitors p21 and p16, arrest proliferation. Such short telomeres, however, retain a sufficient number of telomere-binding proteins to inhibit DNA repair and avoid fusions, and consequently fuel a persistent DNA damage signal that enforces a permanent DNA damage-induced proliferative arrest. This initiates and maintains cellular senescence, a key contributor to organismal ageing and multiple age-related diseases.
This Anniversary Special Issue entitled: "In Honor of Elizabeth Blackburn's 75th Birthday: Celebrating the Discovery of Telomeres", will be dedicated to Prof. Blackburn's achievements and discoveries regarding telomeres in the year of her 75th birthday. Original research papers, reviews and case studies reporting innovative and novel telomere-related research or studies on telomere-related diseases, are herein welcome.
Prof. Dr. Fabrizio D'Adda di Fagagna
Dr. Pawel Kordowitzki
Guest Editors
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