J
Jonathan M. Wastling
Researcher at Keele University
Publications - 120
Citations - 6077
Jonathan M. Wastling is an academic researcher from Keele University. The author has contributed to research in topics: Proteome & Toxoplasma gondii. The author has an hindex of 44, co-authored 119 publications receiving 5492 citations. Previous affiliations of Jonathan M. Wastling include Public Health England & University of Bern.
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Journal ArticleDOI
Proteomic analysis of rhoptry organelles reveals many novel constituents for host-parasite interactions in Toxoplasma gondii
Peter J. Bradley,Peter J. Bradley,Christopher P. Ward,Stephen J. Cheng,David L. Alexander,Susan Coller,Graham H. Coombs,Joe Dan Dunn,David J. P. Ferguson,Sanya J. Sanderson,Jonathan M. Wastling,Jonathan M. Wastling,John C. Boothroyd +12 more
TL;DR: This study developed a method for highly efficient purification of rhoptries from one of the best studied Apicomplexa, Toxoplasma gondii, and carried out a detailed proteomic analysis using mass spectrometry that identified 38 novel proteins that are likely to play a key role in the ability of the parasite to invade and co-opt the host cell for its own survival and growth.
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Comparative Genomics of the Apicomplexan Parasites Toxoplasma gondii and Neospora caninum: Coccidia Differing in Host Range and Transmission Strategy
Adam J. Reid,Sarah J. Vermont,James Cotton,David Harris,Grant A. Hill-Cawthorne,Stephanie Könen-Waisman,Sophia M. Latham,Tobias Mourier,Rebecca Norton,Michael A. Quail,Mandy Sanders,Dhanasekaran Shanmugam,Amandeep Sohal,James D. Wasmuth,James D. Wasmuth,Brian P. Brunk,Michael E. Grigg,Jonathan C. Howard,John Parkinson,David S. Roos,Alexander J. Trees,Matthew Berriman,Arnab Pain,Arnab Pain,Jonathan M. Wastling +24 more
TL;DR: The ecological niches occupied by these species are influenced by a relatively small number of gene products which operate at the host-parasite interface and that the dominance of vertical transmission in N. caninum may be associated with the evolution of reduced virulence in this species.
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The genomic basis of parasitism in the Strongyloides clade of nematodes
Vicky L. Hunt,Isheng J. Tsai,Avril Coghlan,Adam J. Reid,Nancy Holroyd,Bernardo J. Foth,Alan Tracey,James Cotton,Eleanor J Stanley,Helen Beasley,Hayley M. Bennett,Karen Brooks,Bhavana Harsha,Rei Kajitani,Arpita Kulkarni,Dorothee Harbecke,Eiji Nagayasu,Sarah Nichol,Yoshitoshi Ogura,Michael A. Quail,Nadine Randle,Dong Xia,Norbert W. Brattig,Hanns Soblik,Diogo M Ribeiro,Alejandro Sanchez-Flores,Alejandro Sanchez-Flores,Tetsuya Hayashi,Takehiko Itoh,Dee R. Denver,Warwick N. Grant,Jonathan D. Stoltzfus,James B. Lok,Haruhiko Murayama,Jonathan M. Wastling,Jonathan M. Wastling,Adrian Streit,Taisei Kikuchi,Mark Viney,Matthew Berriman +39 more
TL;DR: Exploiting the unique Strongyloides life cycle, the transcriptomes of the parasitic and free-living stages are compared and it is found that these same gene families are upregulated in the parasitic stages, underscoring their role in nematode parasitism.
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The prevalence of anti-Toxoplasma gondii antibodies in Ghanaian sheep and goats.
W.N.A. van der Puije,K.M. Bosompem,E.A. Canacoo,Jonathan M. Wastling,Bartholomew D. Akanmori +4 more
TL;DR: The enzyme-linked immunosorbent assay (ELISA) was used to detect anti-Toxoplasma gondii antibodies in 1258 small ruminants sampled from 28 different locations in the three ecological zones of Ghana and found to be both highly sensitive and specific when compared to the IFAT.
Journal ArticleDOI
Analysis of gene expression from the Wolbachia genome of a filarial nematode supports both metabolic and defensive roles within the symbiosis.
Alistair C. Darby,Stuart D. Armstrong,Germanus S. Bah,Gaganjot Kaur,Margaret Hughes,Suzanne Kay,Pia Koldkjær,Lucille Rainbow,Alan D Radford,Mark Blaxter,Vincent N. Tanya,Alexander J. Trees,Richard Cordaux,Jonathan M. Wastling,Benjamin L. Makepeace +14 more
TL;DR: It is concluded that Wolbachia may have a mitochondrion-like function in the soma, generating ATP for its host, and suggests a role in diverting the immune system toward an ineffective antibacterial response.