Laurence Hurst

Last updated

Laurence Hurst
FRS FMedSci
Professor Laurence Daniel Hurst FMedSci FRS.jpg
Hurst in 2015
Born
Laurence Daniel Hurst

(1965-01-06) 6 January 1965 (age 59) [1]
Ilkley, Yorkshire [1]
Education Truro School [2] [3]
Alma mater
Awards
Scientific career
Fields
Institutions
Thesis Intra-genomic conflict and evolution  (1991)
Doctoral advisor
Doctoral students Gilean McVean [9] [10]
Website go.bath.ac.uk/ldhurst

Laurence Daniel Hurst (born 6 January 1965) [1] FRS FMedSci [11] is a Professor of Evolutionary Genetics in the Department of Biology and Biochemistry at the University of Bath [12] and the director of the Milner Centre for Evolution. [13] [14] [15] [16]

Contents

Education

Hurst was educated at Truro School [1] [2] [3] and the University of Cambridge where he studied the Natural Sciences Tripos at Churchill College, Cambridge, graduating with a Bachelor of Arts degree in 1987. [17] After a year at Harvard University he returned to the UK, and was awarded a Doctor of Philosophy (DPhil) degree from the University of Oxford in 1991 [8] for research supervised by W. D. Hamilton and Alan Grafen. [8]

Career and Research

Hurst was a Royal Society University Research Fellow at the University of Cambridge from 1993 to 1996[ citation needed ] and has been a professor at the University of Bath since 1997. [1]

His research interests [5] include evolution, genetics and genomics using computational and mathematical techniques to understand the way genes and genomes evolve. This has resulted in work on housekeeping genes, [18] gene orders, [19] [20] and the evolution of drug resistance in Staphylococcus aureus , [21] Saccharomyces cerevisiae [22] [23] [24] and the evolution of sexual reproduction / sexual dimorphism. [25]

Hurst works on fundamental problems in the evolution of genetic systems, such as understanding why some sorts of mutations are less damaging than predicted whilst others are more damaging. Mutations that change proteins are, surprisingly, often not especially deleterious. Hurst showed that this was because the genetic code is structured in a way that renders it highly error-proof. Similarly, in applying network representations of gene interactions, he revealed why many deletions of genes have little effect and which deletions tend not to be recessive. [11]

By contrast, Hurst revealed that genomic changes often considered to be relatively harmless – such as gene order changes and mutations at 'silent' sites – are under selection for unanticipated reasons. He also showed how synonymous mutations can disrupt the way gene transcripts are processed. Similarly, in showing that genomes are arranged into gene expression domains, Hurst revealed that genes can affect the expression of other genes in their vicinity. As of 2015 translation of this fundamental work to medicine is a focus of his research. [11]

Awards and honours

Hurst was elected a Fellow of the Academy of Medical Sciences (FMedSci) and a Fellow of the Royal Society (FRS) in 2015. [11] His certificate of election to the Royal Society reads:

Hurst is a leading authority on evolution of genetic systems. He showed that the genetic code is adapted to minimise errors, synonymous mutations in mammals are under selection and gene order is non-random. He was first to recognise the impact of gene expression levels on protein evolution. Hurst spearheaded novel approaches to evolutionary genetics deriving fitness from underlying biochemistry to predict the outcome of laboratory models. This led to fundamental insights into causes of gene dispensability, dominance and variation in gene family size. Hurst, collaborating with cell biologists, identified the human-specific pluripotency gene network and discovered human naïve stem cells. [26]

Hurst was awarded the Scientific Medal of the Zoological Society of London in 2003, [15] and elected a member of European Molecular Biology Organization (EMBO) in 2004. [4] He was awarded The Genetics Society Medal in 2010. [16]

Related Research Articles

<span class="mw-page-title-main">Mutation</span> Alteration in the nucleotide sequence of a genome

In biology, a mutation is an alteration in the nucleic acid sequence of the genome of an organism, virus, or extrachromosomal DNA. Viral genomes contain either DNA or RNA. Mutations result from errors during DNA or viral replication, mitosis, or meiosis or other types of damage to DNA, which then may undergo error-prone repair, cause an error during other forms of repair, or cause an error during replication. Mutations may also result from insertion or deletion of segments of DNA due to mobile genetic elements.

Selfish genetic elements are genetic segments that can enhance their own transmission at the expense of other genes in the genome, even if this has no positive or a net negative effect on organismal fitness. Genomes have traditionally been viewed as cohesive units, with genes acting together to improve the fitness of the organism. However, when genes have some control over their own transmission, the rules can change, and so just like all social groups, genomes are vulnerable to selfish behaviour by their parts.

Molecular evolution describes how inherited DNA and/or RNA change over evolutionary time, and the consequences of this for proteins and other components of cells and organisms. Molecular evolution is the basis of phylogenetic approaches to describing the tree of life. Molecular evolution overlaps with population genetics, especially on shorter timescales. Topics in molecular evolution include the origins of new genes, the genetic nature of complex traits, the genetic basis of adaptation and speciation, the evolution of development, and patterns and processes underlying genomic changes during evolution.

<span class="mw-page-title-main">Neutral theory of molecular evolution</span> Theory of evolution by changes at the molecular level

The neutral theory of molecular evolution holds that most evolutionary changes occur at the molecular level, and most of the variation within and between species are due to random genetic drift of mutant alleles that are selectively neutral. The theory applies only for evolution at the molecular level, and is compatible with phenotypic evolution being shaped by natural selection as postulated by Charles Darwin.

Population genetics is a subfield of genetics that deals with genetic differences within and among populations, and is a part of evolutionary biology. Studies in this branch of biology examine such phenomena as adaptation, speciation, and population structure.

Gene duplication is a major mechanism through which new genetic material is generated during molecular evolution. It can be defined as any duplication of a region of DNA that contains a gene. Gene duplications can arise as products of several types of errors in DNA replication and repair machinery as well as through fortuitous capture by selfish genetic elements. Common sources of gene duplications include ectopic recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage.

Genetic viability is the ability of the genes present to allow a cell, organism or population to survive and reproduce. The term is generally used to mean the chance or ability of a population to avoid the problems of inbreeding. Less commonly genetic viability can also be used in respect to a single cell or on an individual level.

<span class="mw-page-title-main">Conserved sequence</span> Similar DNA, RNA or protein sequences within genomes or among species

In evolutionary biology, conserved sequences are identical or similar sequences in nucleic acids or proteins across species, or within a genome, or between donor and receptor taxa. Conservation indicates that a sequence has been maintained by natural selection.

Neutral mutations are changes in DNA sequence that are neither beneficial nor detrimental to the ability of an organism to survive and reproduce. In population genetics, mutations in which natural selection does not affect the spread of the mutation in a species are termed neutral mutations. Neutral mutations that are inheritable and not linked to any genes under selection will be lost or will replace all other alleles of the gene. That loss or fixation of the gene proceeds based on random sampling known as genetic drift. A neutral mutation that is in linkage disequilibrium with other alleles that are under selection may proceed to loss or fixation via genetic hitchhiking and/or background selection.

<span class="mw-page-title-main">Masatoshi Nei</span> Japanese-American geneticist (1931–2023)

Masatoshi Nei was a Japanese-born American evolutionary biologist.

Evolutionary developmental biology (evo-devo) is the study of developmental programs and patterns from an evolutionary perspective. It seeks to understand the various influences shaping the form and nature of life on the planet. Evo-devo arose as a separate branch of science rather recently. An early sign of this occurred in 1999.

Veronica van Heyningen is an English geneticist who specialises in the etiology of anophthalmia as an honorary professor at University College London (UCL). She previously served as head of medical genetics at the MRC Human Genetics Unit in Edinburgh and the president of The Genetics Society. In 2014 she became president of the Galton Institute. As of 2019 she chairs the diversity committee of the Royal Society, previously chaired by Uta Frith.

<span class="mw-page-title-main">Gil McVean</span> British statistical geneticist (born 1973)

Gilean Alistair Tristram McVean is a professor of statistical genetics at the University of Oxford, fellow of Linacre College, Oxford and co-founder and director of Genomics plc. He also co-chaired the 1000 Genomes Project analysis group.

<span class="mw-page-title-main">Peter Keightley</span>

Peter D. Keightley FRS is Professor of Evolutionary Genetics at the Institute of Evolutionary Biology in School of Biological Sciences at the University of Edinburgh.

<span class="mw-page-title-main">Sarah Teichmann</span> German bioinformatician

Sarah Amalia Teichmann is a German scientist who is head of cellular genetics at the Wellcome Sanger Institute and a visiting research group leader at the European Bioinformatics Institute (EMBL-EBI). She serves as director of research in the Cavendish Laboratory, at the University of Cambridge and a senior research fellow at Churchill College, Cambridge.

<span class="mw-page-title-main">Stephen D. M. Brown</span>

Steve David Macleod Brown is director of the Medical Research Council (MRC) Mammalian Genetics Unit, MRC Harwell at Harwell Science and Innovation Campus, Oxfordshire, a research centre on mouse genetics. In addition, he leads the Genetics and Pathobiology of Deafness research group.

The Extended Evolutionary Synthesis (EES) consists of a set of theoretical concepts argued to be more comprehensive than the earlier modern synthesis of evolutionary biology that took place between 1918 and 1942. The extended evolutionary synthesis was called for in the 1950s by C. H. Waddington, argued for on the basis of punctuated equilibrium by Stephen Jay Gould and Niles Eldredge in the 1980s, and was reconceptualized in 2007 by Massimo Pigliucci and Gerd B. Müller.

<span class="mw-page-title-main">Anne Ferguson-Smith</span> Mammalian developmental geneticist (born 1961)

Anne Carla Ferguson-Smith is a mammalian developmental geneticist. She is the Arthur Balfour Professor of Genetics and Pro-Vice Chancellor for Research and International Partnerships at the University of Cambridge. Formerly head of the Department of Genetics at the University of Cambridge, she is a Fellow of Darwin College, Cambridge and serves as President of the Genetics Society.

In evolutionary biology, developmental bias refers to the production against or towards certain ontogenetic trajectories which ultimately influence the direction and outcome of evolutionary change by affecting the rates, magnitudes, directions and limits of trait evolution. Historically, the term was synonymous with developmental constraint, however, the latter has been more recently interpreted as referring solely to the negative role of development in evolution.

<span class="mw-page-title-main">Csaba Pal</span> Hungarian biologist (born 1975)

Csaba Pal is a Hungarian biologist at the Biological Research Centre (BRC) in Szeged Hungary. His laboratory is part of the Synthetic and Systems Biology Unit at BRC. His research is at the interface of evolution, antibiotic resistance and genome engineering and has published over 80 scientific publications in these areas.

References

  1. 1 2 3 4 5 Anon (2016). "Hurst, Prof. Laurence Daniel" . Who's Who (online Oxford University Press  ed.). Oxford: A & C Black. doi:10.1093/ww/9780199540884.013.U284140.(Subscription or UK public library membership required.)
  2. 1 2 "Laurence Hurst CO83". 18 February 2020.
  3. 1 2 "Alumni gives talk on the weird and wonderful of biology". 14 January 2020.
  4. 1 2 "Find people in the EMBO Communities". people.embo.org.
  5. 1 2 Laurence Hurst publications indexed by Google Scholar OOjs UI icon edit-ltr-progressive.svg
  6. ↑ Hurst, L.; Hamilton, W.; Ladle, R. (1992). "Covert sex". Trends in Ecology & Evolution. 7 (5): 144–145. doi: 10.1016/0169-5347(92)90205-P . PMID   21235987.
  7. ↑ Hurst, L.; Grafen, A. (1990). "Sex and flagellation". Trends in Ecology & Evolution. 5 (12): 419–422. doi:10.1016/0169-5347(90)90029-D. PMID   21232406.
  8. 1 2 3 Hurst, Laurence Daniel (1991). Intra-genomic conflict and evolution (PhD thesis). University of Oxford. OCLC   556449138. EThOS   293434.
  9. ↑ McVean, Gilean Alistair Tristram (1998). Adaptation and conflict: the differences between the sexes in mammalian genome evolution (PhD thesis). University of Cambridge.
  10. ↑ "Students and post-docs past and present in the Hurst laboratory". University of Bath. Archived from the original on 15 May 2015.
  11. 1 2 3 4 "Professor Laurence Hurst FMedSci FRS". London: Royal Society. Archived from the original on 17 November 2015. One or more of the preceding sentences incorporates text from the royalsociety.org website where:
    "All text published under the heading 'Biography' on Fellow profile pages is available under Creative Commons Attribution 4.0 International License." -- "Royal Society Terms, conditions and policies". Archived from the original on 25 September 2015. Retrieved 9 March 2016.{{cite web}}: CS1 maint: bot: original URL status unknown (link)
  12. ↑ 0000-0001-6952-6797 Laurence Hurst publications from Europe PubMed Central
  13. ↑ http://www.bath.ac.uk/bio-sci/research/profiles/hurst-l.html Laurence Hurst at the University of Bath Archived 18 September 2009 at the Wayback Machine
  14. ↑ http://people.bath.ac.uk/bssldh/LaurenceDHurst/Home.html Hurst Laboratory of Evolutionary Genetics and Genomics
  15. 1 2 "Archived copy" (PDF). Archived from the original (PDF) on 17 September 2012. Retrieved 15 June 2011.{{cite web}}: CS1 maint: archived copy as title (link) Zoological Society of London Scientific Medal Winners
  16. 1 2 http://www.genetics.org.uk/page/2775/2010-Genetics-Society-Medal.html 2010 Genetics Society Medal Archived 15 March 2012 at the Wayback Machine
  17. ↑ "Laurence Hurst CV". Archived from the original on 21 March 2012.
  18. ↑ Lercher, M.J.; Urrutia, A.O.; Hurst, L.D. (2002). "Clustering of housekeeping genes provides a unified model of gene order in the human genome". Nature Genetics. 31 (2): 180–183. doi:10.1038/ng887. PMID   11992122. S2CID   5797987.
  19. ↑ Hurst, L.D.; Pál, C.; Lercher, M.J. (2004). "The evolutionary dynamics of eukaryotic gene order". Nature Reviews Genetics. 5 (4): 299–310. doi:10.1038/nrg1319. PMID   15131653. S2CID   5252604.
  20. ↑ Weber, Claudia C; Hurst, Laurence D (2011). "Support for multiple classes of local expression clusters in Drosophila melanogaster, but no evidence for gene order conservation". Genome Biology. 12 (3): R23. doi: 10.1186/gb-2011-12-3-r23 . ISSN   1465-6906. PMC   3129673 . PMID   21414197.
  21. ↑ Holden, M. T. G.; Feil, E.; Lindsay, J.; Peacock, S.; Day, N.; Enright, M.; Foster, T.; Moore, C.; Hurst, L.; Atkin, R.; Barron, A.; Bason, N.; Bentley, S. D.; Chillingworth, C.; Chillingworth, T.; Churcher, C.; Clark, L.; Corton, C.; Cronin, A.; Doggett, J.; Dowd, L.; Feltwell, T.; Hance, Z.; Harris, B.; Hauser, H.; Holroyd, S.; Jagels, K.; James, K. D.; Lennard, N.; Line, A. (2004). "Complete genomes of two clinical Staphylococcus aureus strains: Evidence for the rapid evolution of virulence and drug resistance". Proceedings of the National Academy of Sciences. 101 (26): 9786–9791. Bibcode:2004PNAS..101.9786H. doi: 10.1073/pnas.0402521101 . PMC   470752 . PMID   15213324. Open Access logo PLoS transparent.svg
  22. ↑ Papp, Balázs; Pál, Csaba; Hurst, Laurence D. (2003). "Dosage sensitivity and the evolution of gene families in yeast". Nature. 424 (6945): 194–197. Bibcode:2003Natur.424..194P. doi:10.1038/nature01771. ISSN   0028-0836. PMID   12853957. S2CID   4382441.
  23. ↑ Pál, C.; Papp, B.; Hurst, L. (2001). "Highly expressed genes in yeast evolve slowly". Genetics. 158 (2): 927–931. doi:10.1093/genetics/158.2.927. PMC   1461684 . PMID   11430355.
  24. ↑ Weber, C. C.; Hurst, L. D. (2009). "Protein Rates of Evolution Are Predicted by Double-Strand Break Events, Independent of Crossing-over Rates". Genome Biology and Evolution. 1: 340–349. doi:10.1093/gbe/evp033. PMC   2817428 . PMID   20333203.
  25. ↑ Hurst, Laurence D.; Peck, Joel R. (1996). "Recent advances in understanding of the evolution and maintenance of sex". Trends in Ecology & Evolution. 11 (2): 46–52. doi:10.1016/0169-5347(96)81041-X. ISSN   0169-5347. PMID   21237760.
  26. ↑ "Certificate of election: EC/2015/24". London: Royal Society. Archived from the original on 20 December 2015.
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