Robert Hirt

Prof. Robert Hirt

Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK
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Research Focus & Metrics

Academic Career Length

35Years (1992-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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12 January 2007 in Science
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JCJane M. Carlton
Jane M. Carlton
RHRobert Hirt
Robert Hirt
JSJoana C. Silva
Joana C. Silva
ADArthur L. Delcher
Arthur L. Delcher
MSMichael Schatz
Michael Schatz
PJPatricia J. Johnson
Patricia J. Johnson
We describe the genome sequence of the protist Trichomonas vaginalis , a sexually transmitted human pathogen. Repeats and transposable elements comprise about two-thirds of the ∼160-megabase genome, reflecting a recent massive expansion of genetic material. This expansion, in conjunction with the shaping of metabolic pathways that likely transpired through lateral gene transfer from bacteria, and amplification of specific gene families implicated in pathogenesis and phagocytosis of host proteins may exemplify adaptations of the parasite during its transition to a urogenital environment. The genome sequence predicts previously unknown functions for the hydrogenosome, which support a common evolutionary origin of this unusual organelle with mitochondria.

1 February 2005 in Nature
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Brendan LoftusBrendan Loftus
Brendan Loftus
IAIain Anderson
Iain Anderson
RDRob Davies
Rob Davies
UAU. Cecilia M. Alsmark
U. Cecilia M. Alsmark
JSJohn Samuelson
John Samuelson
NHNeil Hall
Neil Hall
Entamoeba histolytica is an intestinal parasite and the causative agent of amoebiasis, which is a significant source of morbidity and mortality in developing countries1. Here we present the genome of E. histolytica, which reveals a variety of metabolic adaptations shared with two other amitochondrial protist pathogens: Giardia lamblia and Trichomonas vaginalis. These adaptations include reduction or elimination of most mitochondrial metabolic pathways and the use of oxidative stress enzymes generally associated with anaerobic prokaryotes. Phylogenomic analysis identifies evidence for lateral gene transfer of bacterial genes into the E. histolytica genome, the effects of which centre on expanding aspects of E. histolytica's metabolic repertoire. The presence of these genes and the potential for novel metabolic pathways in E. histolytica may allow for the development of new chemotherapeutic agents. The genome encodes a large number of novel receptor kinases and contains expansions of a variety of gene families, including those associated with virulence. Additional genome features include an abundance of tandemly repeated transfer-RNA-containing arrays, which may have a structural function in the genome. Analysis of the genome provides new insights into the workings and genome evolution of a major human pathogen.

19 January 1999 in Proceedings of the National Academy of Sciences
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RHRobert Hirt
Robert Hirt
JLJohn M. Logsdon
John M. Logsdon
BHBryan Healy
Bryan Healy
MDMichael W. Dorey
Michael W. Dorey
WDW. Ford Doolittle
W. Ford Doolittle
TET. Martin Embley
T. Martin Embley
We have determined complete gene sequences encoding the largest subunit of the RNA polymerase II (RBP1) from two Microsporidia, Vairimorpha necatrix and Nosema locustae . Phylogenetic analyses of these and other RPB1 sequences strongly support the notion that Microsporidia are not early-diverging eukaryotes but instead are specifically related to Fungi. Our reexamination of elongation factors EF-1α and EF-2 sequence data that had previously been taken as support for an early (Archezoan) divergence of these amitochondriate protists show such support to be weak and likely caused by artifacts in phylogenetic analyses. These EF data sets are, in fact, not inconsistent with a Microsporidia + Fungi relationship. In addition, we show that none of these proteins strongly support a deep divergence of Parabasalia and Metamonada, the other amitochondriate protist groups currently thought to compose early branches. Thus, the phylogenetic placement among eukaryotes for these protist taxa is in need of further critical examination.

1 August 2002 in Nature
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BWBryony Williams
Bryony Williams
RHRobert Hirt
Robert Hirt
John LucocqJohn Lucocq
John Lucocq
TET. Martin Embley
T. Martin Embley

23 December 2008 in Proceedings of the National Academy of Sciences
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CCCymon J. Cox
Cymon J. Cox
PFPeter G. Foster
Peter G. Foster
RHRobert Hirt
Robert Hirt
SHSimon R. Harris
Simon R. Harris
TET. Martin Embley
T. Martin Embley
The origin of the eukaryotic genetic apparatus is thought to be central to understanding the evolution of the eukaryotic cell. Disagreement about the source of the relevant genes has spawned competing hypotheses for the origins of the eukaryote nuclear lineage. The iconic rooted 3-domains tree of life shows eukaryotes and archaebacteria as separate groups that share a common ancestor to the exclusion of eubacteria. By contrast, the eocyte hypothesis has eukaryotes originating within the archaebacteria and sharing a common ancestor with a particular group called theCrenarchaeotaor eocytes. Here, we have investigated the relative support for each hypothesis from analysis of 53 genes spanning the 3 domains, including essential components of the eukaryotic nucleic acid replication, transcription, and translation apparatus. As an important component of our analysis, we investigated the fit between model and data with respect to composition. Compositional heterogeneity is a pervasive problem for reconstruction of ancient relationships, which, if ignored, can produce an incorrect tree with strong support. To mitigate its effects, we used phylogenetic models that allow for changing nucleotide or amino acid compositions over the tree and data. Our analyses favor a topology that supports the eocyte hypothesis rather than archaebacterial monophyly and the 3-domains tree of life.

30 April 2008 in Nature
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ATAnastasios D. Tsaousis
Anastasios D. Tsaousis
EKEdmund R.S. Kunji
Edmund R.S. Kunji
AGAlina V. Goldberg
Alina V. Goldberg
John LucocqJohn Lucocq
John Lucocq
RHRobert Hirt
Robert Hirt
TET. Martin Embley
T. Martin Embley