Joseph Thornton (biologist)

Last updated
Joe Thornton
Born
Chicago, IL
Citizenship United States
Alma mater Yale University, Columbia University
Known forhis work on molecular evolution
Awards NCSE Friend of Darwin Award (2019), [1] U.S. Presidential Early Career Award for Scientists and Engineers (2007), Howard Hughes Medical Institute Early Career Scientist Award (2009), National Science Foundation (2006)
Scientific career
Fields Evolutionary biology
Institutions University of Oregon , University of Chicago

Joseph (Joe) Thornton is an American Biologist. He is a Professor at the University of Chicago and a former Early Career Scientist of the Howard Hughes Medical Institute. He is known for resurrecting ancestral genes and tracing the mechanisms by which proteins evolve new functions. [2] [3] [4] [5] [6] [7] [8]

His work has been discussed in arguments concerning intelligent design and "irreducible complexity." [9] [10] [11] [12] [13] [14] [15] It has also been featured in popular discussions of the contingency of evolution. [16] [17] [18]

Thornton has received the U.S. Presidential Early Career Award for Scientists and Engineers at the White House, as well as a Career Award from the National Science Foundation and an Early Career Scientist Award from the Howard Hughes Medical Institute.

His background and career were profiled in an article in the journal Nature, which focused on his unusual path into science, including undergraduate study as an English major and several years as an environmental activist working for Greenpeace. [19]

Related Research Articles

Olfactory receptors (ORs), also known as odorant receptors, are chemoreceptors expressed in the cell membranes of olfactory receptor neurons and are responsible for the detection of odorants which give rise to the sense of smell. Activated olfactory receptors trigger nerve impulses which transmit information about odor to the brain. These receptors are members of the class A rhodopsin-like family of G protein-coupled receptors (GPCRs). The olfactory receptors form a multigene family consisting of around 800 genes in humans and 1400 genes in mice.

Dollos law of irreversibility Hypothesis by Louis Dollo in 1893, which states evolution is not exactly reversible

Dollo's law of irreversibility, proposed in 1893 by Belgian paleontologist Louis Dollo states that, "an organism never returns exactly to a former state, even if it finds itself placed in conditions of existence identical to those in which it has previously lived ... it always keeps some trace of the intermediate stages through which it has passed."

Estrogen receptor Proteins activated by the hormone estrogen

Estrogen receptors (ERs) are a group of proteins found inside cells. They are receptors that are activated by the hormone estrogen (17β-estradiol). Two classes of ER exist: nuclear estrogen receptors, which are members of the nuclear receptor family of intracellular receptors, and membrane estrogen receptors (mERs), which are mostly G protein-coupled receptors. This article refers to the former (ER).

Estrogen receptor alpha Protein-coding gene in the species Homo sapiens

Estrogen receptor alpha (ERα), also known as NR3A1, is one of two main types of estrogen receptor, a nuclear receptor that is activated by the sex hormone estrogen. In humans, ERα is encoded by the gene ESR1.

Nuclear receptor Protein

In the field of molecular biology, nuclear receptors are a class of proteins found within cells that are responsible for sensing steroid and thyroid hormones and certain other molecules. In response, these receptors work with other proteins to regulate the expression of specific genes, thereby controlling the development, homeostasis, and metabolism of the organism.

The ERRs are orphan nuclear receptors, meaning the identity of their endogenous ligand has yet to be unambiguously determined. They are named because of sequence homology with estrogen receptors, but do not appear to bind estrogens or other tested steroid hormones.

Nuclear receptor coactivator 3

The nuclear receptor coactivator 3 also known as NCOA3 is a protein that, in humans, is encoded by the NCOA3 gene. NCOA3 is also frequently called 'amplified in breast 1' (AIB1), steroid receptor coactivator-3 (SRC-3), or thyroid hormone receptor activator molecule 1 (TRAM-1).

Estrogen-related receptor alpha Protein-coding gene in the species Homo sapiens

Estrogen-related receptor alpha (ERRα), also known as NR3B1, is a nuclear receptor that in humans is encoded by the ESRRA gene. ERRα was originally cloned by DNA sequence homology to the estrogen receptor alpha, but subsequent ligand binding and reporter-gene transfection experiments demonstrated that estrogens did not regulate ERRα. Currently, ERRα is considered an orphan nuclear receptor.

Testicular receptor 4

Testicular receptor 4 also known as NR2C2 is a protein that in humans is encoded by the NR2C2 gene.

OR1D2

Olfactory receptor 1D2 is a protein that in humans is encoded by the OR1D2 gene.

MED1

Mediator of RNA polymerase II transcription subunit 1 also known as DRIP205 or Trap220 is a subunit of the Mediator complex and is a protein that in humans is encoded by the MED1 gene. MED1 functions as a nuclear receptor coactivator.

MED24

Mediator of RNA polymerase II transcription subunit 24 is an enzyme that in humans is encoded by the MED24 gene.

CRSP3

Mediator of RNA polymerase II transcription subunit 23 is an enzyme that in humans is encoded by the MED23 gene.

PHB2

Prohibitin-2 is a protein that in humans is encoded by the PHB2 gene.

PTPRG

Receptor-type tyrosine-protein phosphatase gamma is an enzyme that in humans is encoded by the PTPRG gene.

Within biological systems, degeneracy occurs when structurally dissimilar components/modules/pathways can perform similar functions under certain conditions, but perform distinct functions in other conditions. Degeneracy is thus a relational property that requires comparing the behavior of two or more components. In particular, if degeneracy is present in a pair of components, then there will exist conditions where the pair will appear functionally redundant but other conditions where they will appear functionally distinct.

James A. Lake is an American evolutionary biologist and a Distinguished Professor of Molecular, Cell, and Developmental Biology and of Human Genetics at UCLA. Lake is best known for the New Animal Phylogeny and for the first three-dimensional structure of the ribosome. He has also made significant contributions to understanding genome evolution across all kingdoms of life, including discovering informational and operational genes, elucidating the complexity hypothesis for gene transfer, rooting the tree of life, and understanding the early transition from prokaryotic to eukaryotic life.

Enzyme promiscuity is the ability of an enzyme to catalyse a fortuitous side reaction in addition to its main reaction. Although enzymes are remarkably specific catalysts, they can often perform side reactions in addition to their main, native catalytic activity. These promiscuous activities are usually slow relative to the main activity and are under neutral selection. Despite ordinarily being physiologically irrelevant, under new selective pressures these activities may confer a fitness benefit therefore prompting the evolution of the formerly promiscuous activity to become the new main activity. An example of this is the atrazine chlorohydrolase from Pseudomonas sp. ADP that evolved from melamine deaminase, which has very small promiscuous activity toward atrazine, a man-made chemical.

Ancestral sequence reconstruction (ASR) – also known as ancestral gene/sequence reconstruction/resurrection – is a technique used in the study of molecular evolution. The method uses related sequences to reconstruct an "ancestral" gene from a multiple sequence alignment.

Epistasis Dependence of a gene mutations phenotype on mutations in other genes

Epistasis is a phenomenon in genetics in which the effect of a gene mutation is dependent on the presence or absence of mutations in one or more other genes, respectively termed modifier genes. In other words, the effect of the mutation is dependent on the genetic background in which it appears. Epistatic mutations therefore have different effects on their own than when they occur together. Originally, the term epistasis specifically meant that the effect of a gene variant is masked by that of a different gene.

References

  1. ↑ Branch, Glenn (23 May 2019). "Friend of Darwin and Friend of the Planet awards for 2019". Archived from the original on 2019-06-11. Retrieved 2019-06-14.
  2. ↑ Dean, A. M.; Thornton, J. W. (2007). "Mechanistic approaches to the study of evolution: The functional synthesis". Nature Reviews Genetics. 8 (9): 675–88. doi:10.1038/nrg2160. PMC   2488205 . PMID   17703238.
  3. ↑ Finnigan, G. C.; Hanson-Smith, V.; Stevens, T. H.; Thornton, J. W. (2012). "Evolution of increased complexity in a molecular machine". Nature. 481 (7381): 360–4. Bibcode:2012Natur.481..360F. doi:10.1038/nature10724. PMC   3979732 . PMID   22230956.
  4. ↑ Thornton, J. W.; Carroll, S. M. (2011). "Lamprey endocrinology is not ancestral". Proceedings of the National Academy of Sciences. 108 (2): E5. Bibcode:2011PNAS..108E...5T. doi: 10.1073/pnas.1014896108 . PMC   3021036 . PMID   21209326.
  5. ↑ Ortlund, E. A.; Bridgham, J. T.; Redinbo, M. R.; Thornton, J. W. (2007). "Crystal structure of an ancient protein: Evolution by conformational epistasis". Science. 317 (5844): 1544–1548. Bibcode:2007Sci...317.1544O. doi:10.1126/science.1142819. PMC   2519897 . PMID   17702911.
  6. ↑ Thornton, J. W. (2001). "Evolution of vertebrate steroid receptors from an ancestral estrogen receptor by ligand exploitation and serial genome expansions". Proceedings of the National Academy of Sciences. 98 (10): 5671–5676. Bibcode:2001PNAS...98.5671T. doi: 10.1073/pnas.091553298 . PMC   33271 . PMID   11331759.
  7. ↑ Hawkins, M. B.; Thornton, J. W.; Crews, D.; Skipper, J. K.; Dotte, A.; Thomas, P. (2000). "Identification of a third distinct estrogen receptor and reclassification of estrogen receptors in teleosts". Proceedings of the National Academy of Sciences of the United States of America. 97 (20): 10751–10756. Bibcode:2000PNAS...9710751H. doi: 10.1073/pnas.97.20.10751 . PMC   27095 . PMID   11005855.
  8. ↑ Bridgham, J. T.; Ortlund, E. A.; Thornton, J. W. (2009). "An epistatic ratchet constrains the direction of glucocorticoid receptor evolution". Nature. 461 (7263): 515–519. Bibcode:2009Natur.461..515B. doi:10.1038/nature08249. PMC   6141187 . PMID   19779450.
  9. ↑ Chang, Kenneth (April 7, 2006). "Study, in a First, Explains Evolution's Molecular Advance". New York Times. New York.
  10. ↑ Begley, Sharon (April 7, 2006). "Two New Discoveries Answer Big Questions in Evolution Theory". Wall Street Journal. New York.
  11. ↑ Adami, C. (2006). "EVOLUTION: Reducible Complexity". Science. 312 (5770): 61–63. doi:10.1126/science.1126559. PMID   16601180. S2CID   8452876.
  12. ↑ Zimmer, Carl. "The Blind Locksmith Continued: An Update from Joe Thornton". The Loom. Discover Magazine.
  13. ↑ Zimmer, Carl. "The Blind Locksmith". The Loom. Discover Magazine.
  14. ↑ Begley, Sharon. "One less gap for god of the gaps". Lab Notes. Newsweek. Archived from the original on 2013-01-04.
  15. ↑ Matheson, Steven (2007-10-15). "How to evolve a new protein in (about) 8 esy steps". Quintessence of Dust.
  16. ↑ Chang, Kenneth (August 21, 2007). "Ancient Protein Tells a Story of Changing Functions". New York Times. New York.
  17. ↑ Zimmer, Carl (September 28, 2009). "Can Evolution Run in Reverse? A Study Says It's a One-Way Street". New York Times. New York.
  18. ↑ "No Going Back (editorial)". New York Times. New York. October 6, 2009.
  19. ↑ Pearson, Helen (March 21, 2012). "Prehistoric proteins: Raising the dead". Nature. London.
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