Carol W. Greider employer Johns Hopkins University
Subsequent career
Greider then started her own laboratory as a Cold Spring Harbor Laboratory Fellow, and also held a faculty position, at the Cold Spring Harbor Laboratory, Long Island, New York. Greider continued to study Tetrahymena telomerase, cloning the gene encoding the RNA component and demonstrating that it provided the template for the TTGGGG telomere repeats (1989)  as well as establishing that telomerase is processive (1991). She was also able to reconstitute Tetrahymena telomerase in vitro (1994) and define the mechanisms of template utilization (1995). Greider also worked with Calvin Harley to show that telomere shortening underlies cellular senescence (1990). To further test this idea mouse and human telomerase were characterized (1993) (1995) and the mouse telomerase RNA component was cloned (1995).During this time, Greider, in collaboration with Ronald A. DePinho, produced the first telomerase knockout mouse, showing that although telomerase is dispensable for life, increasingly short telomeres result in various deleterious phenotypes, colloquially referred to as premature aging. In the mid-1990s, Greider was recruited by Michael D. West, founder of biotechnology company Geron (now CEO of AgeX Therapeutics) to join the company's Scientific Advisory Board and remained on the Board until 1997.
Greider accepted a faculty position at the Johns Hopkins University School of Medicine in 1997. Greider continued to study telomerase deficient mice and saw that her sixth generation of mice had become entirely sterile, but when mated with control mice the telomerase deficient mice were able to regenerate their telomeres. Greider continued to work on telomerase biochemistry, defining the secondary structure (2000)  and template boundary (2003) of vertebrate telomerase RNA as well as analyzing the pseudoknot structure in human telomerase RNA (2005). In addition to working in Tetrahymena and mammalian systems, Greider also studied telomeres and telomerase in the yeast Saccharomyces cerevisiae, further characterizing the recombination-based gene conversion mechanism that yeast cells null for telomerase use to maintain telomeres (1999) (2001). Greider also showed that short telomeres elicit a DNA damage response in yeast (2003).Greider, Blackburn, and Szostak shared the 2006 Albert Lasker Award for Basic Medical Research for their work on telomeres, before jointly receiving the Nobel Prize in 2009.
In February 2014, Greider was named a Bloomberg Distinguished Professor at Johns Hopkins University.Greider served as director of and professor at the Department of Molecular Biology and Genetics at Johns Hopkins Medicine. Greider was first promoted to Daniel Nathans Professor at the Department of Molecular Biology and Genetics in 2004.As of 2021, she is a professor of molecular, cellular, and developmental biology at UCSC.Greider's lab employs both student and post-doctoral trainees to further examine the relationships between the biology of telomeres and their connection to disease. Greider's lab uses a variety of tools including yeast, mice, and biochemistry to look at progressive telomere shortening. Greider's lab is also researching how tumor reformation can be controlled by the presence of short telomeres. The lab's future work will focus more on identifying the processing and regulation of telomeres and telomere elongation.
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