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Stuart Armstrong
Institute of Infection and Global Health, University of Liverpool, Liverpool Science Park IC2, Liverpool L3 5RF, UK

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Journal article
Published: 15 May 2021 in Viruses
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Arboviruses such as bluetongue virus (BTV) replicate in arthropod vectors involved in their transmission between susceptible vertebrate-hosts. The “classical” BTV strains infect and replicate effectively in cells of their insect-vectors (Culicoides biting-midges), as well as in those of their mammalian-hosts (ruminants). However, in the last decade, some “atypical” BTV strains, belonging to additional serotypes (e.g., BTV-26), have been found to replicate efficiently only in mammalian cells, while their replication is severely restricted in Culicoides cells. Importantly, there is evidence that these atypical BTV are transmitted by direct-contact between their mammalian hosts. Here, the viral determinants and mechanisms restricting viral replication in Culicoides were investigated using a classical BTV-1, an “atypical” BTV-26 and a BTV-1/BTV-26 reassortant virus, derived by reverse genetics. Viruses containing the capsid of BTV-26 showed a reduced ability to attach to Culicoides cells, blocking early steps of the replication cycle, while attachment and replication in mammalian cells was not restricted. The replication of BTV-26 was also severely reduced in other arthropod cells, derived from mosquitoes or ticks. The data presented identifies mechanisms and potential barriers to infection and transmission by the newly emerged “atypical” BTV strains in Culicoides.

ACS Style

Marc Guimerà Busquets; Gillian Pullinger; Karin Darpel; Lyndsay Cooke; Stuart Armstrong; Jennifer Simpson; Massimo Palmarini; Rennos Fragkoudis; Peter Mertens. An Early Block in the Replication of the Atypical Bluetongue Virus Serotype 26 in Culicoides Cells Is Determined by Its Capsid Proteins. Viruses 2021, 13, 919 .

AMA Style

Marc Guimerà Busquets, Gillian Pullinger, Karin Darpel, Lyndsay Cooke, Stuart Armstrong, Jennifer Simpson, Massimo Palmarini, Rennos Fragkoudis, Peter Mertens. An Early Block in the Replication of the Atypical Bluetongue Virus Serotype 26 in Culicoides Cells Is Determined by Its Capsid Proteins. Viruses. 2021; 13 (5):919.

Chicago/Turabian Style

Marc Guimerà Busquets; Gillian Pullinger; Karin Darpel; Lyndsay Cooke; Stuart Armstrong; Jennifer Simpson; Massimo Palmarini; Rennos Fragkoudis; Peter Mertens. 2021. "An Early Block in the Replication of the Atypical Bluetongue Virus Serotype 26 in Culicoides Cells Is Determined by Its Capsid Proteins." Viruses 13, no. 5: 919.

Journal article
Published: 14 October 2020 in Viruses
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of coronavirus disease 2019 (COVID-19). Sequencing the viral genome as the outbreak progresses is important, particularly in the identification of emerging isolates with different pathogenic potential and to identify whether nucleotide changes in the genome will impair clinical diagnostic tools such as real-time PCR assays. Although single nucleotide polymorphisms and point mutations occur during the replication of coronaviruses, one of the biggest drivers in genetic change is recombination. This can manifest itself in insertions and/or deletions in the viral genome. Therefore, sequencing strategies that underpin molecular epidemiology and inform virus biology in patients should take these factors into account. A long amplicon/read length-based RT-PCR sequencing approach focused on the Oxford Nanopore MinION/GridION platforms was developed to identify and sequence the SARS-CoV-2 genome in samples from patients with or suspected of COVID-19. The protocol, termed Rapid Sequencing Long Amplicons (RSLAs) used random primers to generate cDNA from RNA purified from a sample from a patient, followed by single or multiplex PCRs to generate longer amplicons of the viral genome. The base protocol was used to identify SARS-CoV-2 in a variety of clinical samples and proved sensitive in identifying viral RNA in samples from patients that had been declared negative using other nucleic acid-based assays (false negative). Sequencing the amplicons revealed that a number of patients had a proportion of viral genomes with deletions.

ACS Style

Shona C. Moore; Rebekah Penrice-Randall; Muhannad Alruwaili; Nadine Randle; Stuart Armstrong; Catherine Hartley; Sam Haldenby; Xiaofeng Dong; Abdulrahman Alrezaihi; Mai Almsaud; Eleanor Bentley; Jordan Clark; Isabel García-Dorival; Paul Gilmore; Ximeng Han; Benjamin Jones; Lisa Luu; Parul Sharma; Ghada Shawli; Yani Sun; Qin Zhao; Steven T. Pullan; Daniel P. Carter; Kevin Bewley; Jake Dunning; En-Min Zhou; Tom Solomon; Michael Beadsworth; James Cruise; Derrick W. Crook; David A. Matthews; Andrew D. Davidson; Zana Mahmood; Waleed Aljabr; Julian Druce; Richard Vipond; Lisa Ng; Laurent Renia; Peter J. M. Openshaw; J. Kenneth Baillie; Miles W. Carroll; James Stewart; Alistair Darby; Malcolm Semple; Lance Turtle; Julian A. Hiscox. Amplicon-Based Detection and Sequencing of SARS-CoV-2 in Nasopharyngeal Swabs from Patients With COVID-19 and Identification of Deletions in the Viral Genome That Encode Proteins Involved in Interferon Antagonism. Viruses 2020, 12, 1164 .

AMA Style

Shona C. Moore, Rebekah Penrice-Randall, Muhannad Alruwaili, Nadine Randle, Stuart Armstrong, Catherine Hartley, Sam Haldenby, Xiaofeng Dong, Abdulrahman Alrezaihi, Mai Almsaud, Eleanor Bentley, Jordan Clark, Isabel García-Dorival, Paul Gilmore, Ximeng Han, Benjamin Jones, Lisa Luu, Parul Sharma, Ghada Shawli, Yani Sun, Qin Zhao, Steven T. Pullan, Daniel P. Carter, Kevin Bewley, Jake Dunning, En-Min Zhou, Tom Solomon, Michael Beadsworth, James Cruise, Derrick W. Crook, David A. Matthews, Andrew D. Davidson, Zana Mahmood, Waleed Aljabr, Julian Druce, Richard Vipond, Lisa Ng, Laurent Renia, Peter J. M. Openshaw, J. Kenneth Baillie, Miles W. Carroll, James Stewart, Alistair Darby, Malcolm Semple, Lance Turtle, Julian A. Hiscox. Amplicon-Based Detection and Sequencing of SARS-CoV-2 in Nasopharyngeal Swabs from Patients With COVID-19 and Identification of Deletions in the Viral Genome That Encode Proteins Involved in Interferon Antagonism. Viruses. 2020; 12 (10):1164.

Chicago/Turabian Style

Shona C. Moore; Rebekah Penrice-Randall; Muhannad Alruwaili; Nadine Randle; Stuart Armstrong; Catherine Hartley; Sam Haldenby; Xiaofeng Dong; Abdulrahman Alrezaihi; Mai Almsaud; Eleanor Bentley; Jordan Clark; Isabel García-Dorival; Paul Gilmore; Ximeng Han; Benjamin Jones; Lisa Luu; Parul Sharma; Ghada Shawli; Yani Sun; Qin Zhao; Steven T. Pullan; Daniel P. Carter; Kevin Bewley; Jake Dunning; En-Min Zhou; Tom Solomon; Michael Beadsworth; James Cruise; Derrick W. Crook; David A. Matthews; Andrew D. Davidson; Zana Mahmood; Waleed Aljabr; Julian Druce; Richard Vipond; Lisa Ng; Laurent Renia; Peter J. M. Openshaw; J. Kenneth Baillie; Miles W. Carroll; James Stewart; Alistair Darby; Malcolm Semple; Lance Turtle; Julian A. Hiscox. 2020. "Amplicon-Based Detection and Sequencing of SARS-CoV-2 in Nasopharyngeal Swabs from Patients With COVID-19 and Identification of Deletions in the Viral Genome That Encode Proteins Involved in Interferon Antagonism." Viruses 12, no. 10: 1164.

Other
Published: 04 July 2020
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Background Tissue inflammation is associated with organ dysfunction and death in Covid-19. The efficacy of dexamethasone in preventing mortality in critical Covid-19 suggests that inflammation has a causal role in death. Whether this deleterious inflammation is a direct response to the presence of SARS-CoV-2, or an independent immuno-pathologic process, is unknown. Methods Tissue was acquired from detailed post-mortem examinations conducted on 11 well characterised hospitalised patients with fatal Covid-19. SARS-CoV-2 organotropism was mapped at an organ level by multiplex PCR and sequencing, with cellular resolution achieved by in situ viral spike (S) protein detection. Histological evidence of inflammation and organ injury was systematically examined, and the pulmonary immune response characterized with multiplex immunofluorescence. Findings SARS-CoV-2 was detected across a wide variety of organs, most frequently in the respiratory tract but also in numerous extra-pulmonary sites. Minimal histological evidence of inflammation was identified in non-pulmonary organs despite frequent detection of viral RNA and protein. At a cellular level, viral protein was identified without adjacent inflammation in the intestine, liver and kidney. Severe inflammatory change was restricted to the lung and reticulo-endothelial system. Diffuse alveolar damage, pulmonary thrombi and a monocyte/myeloid-predominant vasculitis were the predominant pulmonary findings, though there was not a consistent association between viral presence and either the presence or nature of the inflammatory response within the lung. Immunophenotyping revealed an influx of macrophages, monocytes and T cells into pulmonary parenchyma. Bone marrow examination revealed plasmacytosis, erythroid dysplasia and iron-laden macrophages. Plasma cell excess was also present in lymph node, spleen and lung. These stereotyped reticulo-endothelial responses occurred largely independently of the presence of virus in lymphoid tissues. Conclusions Tissue inflammation and organ dysfunction in fatal Covid-19 do not map to the tissue and cellular distribution of SARS-CoV-2, demonstrating tissue-specific tolerance. We conclude that death in Covid-19 is primarily a consequence of immune-mediated, rather than pathogen-mediated, organ inflammation and injury. Funding The Chief Scientist Office, LifeArc, Medical Research Scotland, UKRI (MRC).

ACS Style

David A Dorward; Clark D Russell; In Hwa Um; Mustafa Elshani; Stuart D Armstrong; Rebekah Penrice-Randal; Tracey Millar; Chris Eb Lerpiniere; Giulia Tagliavini; Catherine S Hartley; Nadine P Randall; Naomi N Gachanja; Philippe Md Potey; Alison M Anderson; Victoria L Campbell; Alasdair J Duguid; Wael Al Qsous; Ralph Bouhaidar; J Kenneth Baillie; Kevin Dhaliwal; William A Wallace; Christopher Oc Bellamy; Sandrine Prost; Colin Smith; Julian A Hiscox; David J Harrison; Christopher D Lucas. Tissue-specific tolerance in fatal Covid-19. 2020, 1 .

AMA Style

David A Dorward, Clark D Russell, In Hwa Um, Mustafa Elshani, Stuart D Armstrong, Rebekah Penrice-Randal, Tracey Millar, Chris Eb Lerpiniere, Giulia Tagliavini, Catherine S Hartley, Nadine P Randall, Naomi N Gachanja, Philippe Md Potey, Alison M Anderson, Victoria L Campbell, Alasdair J Duguid, Wael Al Qsous, Ralph Bouhaidar, J Kenneth Baillie, Kevin Dhaliwal, William A Wallace, Christopher Oc Bellamy, Sandrine Prost, Colin Smith, Julian A Hiscox, David J Harrison, Christopher D Lucas. Tissue-specific tolerance in fatal Covid-19. . 2020; ():1.

Chicago/Turabian Style

David A Dorward; Clark D Russell; In Hwa Um; Mustafa Elshani; Stuart D Armstrong; Rebekah Penrice-Randal; Tracey Millar; Chris Eb Lerpiniere; Giulia Tagliavini; Catherine S Hartley; Nadine P Randall; Naomi N Gachanja; Philippe Md Potey; Alison M Anderson; Victoria L Campbell; Alasdair J Duguid; Wael Al Qsous; Ralph Bouhaidar; J Kenneth Baillie; Kevin Dhaliwal; William A Wallace; Christopher Oc Bellamy; Sandrine Prost; Colin Smith; Julian A Hiscox; David J Harrison; Christopher D Lucas. 2020. "Tissue-specific tolerance in fatal Covid-19." , no. : 1.

Journal article
Published: 10 October 2019 in Viruses
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Human respiratory syncytial virus (HRSV) is a major cause of pediatric infection and also causes disease in the elderly and those with underlying respiratory problems. There is no vaccine for HRSV and anti-viral therapeutics are not broadly applicable. To investigate the effect of HRSV biology in children, nasopharyngeal aspirates were taken from children with different viral loads and a combined high throughput RNAseq and label free quantitative proteomics approach was used to characterize the nucleic acid and proteins in these samples. HRSV proteins were identified in the nasopharyngeal aspirates from infected children, and their abundance correlated with viral load (Ct value), confirming HRSV infection. Analysis of the HRSV genome indicated that the children were infected with sub-group A virus and that minor variants in nucleotide frequency occurred in discrete clusters along the HRSV genome, and within a patient clustered distinctly within the glycoprotein gene. Data from the samples were binned into four groups; no-HRSV infection (control), high viral load (Ct < 20), medium viral load (Ct = 20-25), and low viral load (Ct > 25). Cellular proteins associated with the anti-viral response (e.g., ISG15) were identified in the nasopharyngeal aspirates and their abundance was correlated with viral load. These combined approaches have not been used before to study HRSV biology in vivo and can be readily applied to the study the variation of virus host interactions.

ACS Style

Waleed Aljabr; Stuart Armstrong; Natasha Y. Rickett; Georgios Pollakis; Olivier Touzelet; Elaine Cloutman-Green; David A. Matthews; Julian A. Hiscox. High Resolution Analysis of Respiratory Syncytial Virus Infection In Vivo. Viruses 2019, 11, 926 .

AMA Style

Waleed Aljabr, Stuart Armstrong, Natasha Y. Rickett, Georgios Pollakis, Olivier Touzelet, Elaine Cloutman-Green, David A. Matthews, Julian A. Hiscox. High Resolution Analysis of Respiratory Syncytial Virus Infection In Vivo. Viruses. 2019; 11 (10):926.

Chicago/Turabian Style

Waleed Aljabr; Stuart Armstrong; Natasha Y. Rickett; Georgios Pollakis; Olivier Touzelet; Elaine Cloutman-Green; David A. Matthews; Julian A. Hiscox. 2019. "High Resolution Analysis of Respiratory Syncytial Virus Infection In Vivo." Viruses 11, no. 10: 926.

Preprint
Published: 26 November 2018
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Major urinary proteins (MUP) are the major component of the urinary protein fraction in house mice (Mus spp.) and rats (Rattus spp.). The structure, polymorphism and functions of these lipocalins have been well described in the western European house mouse (Mus musculus domesticus), clarifying their role in semiochemical communication. The complexity of these roles in the mouse raises the question of similar functions in other rodents, including the Norway rat, Rattus norvegicus. Norway rats express MUPs in urine but information about specific MUP isoform sequences and functions is limited. In this study, we present a detailed molecular characterization of the MUP proteoforms expressed in the urine of two laboratory strains, Wistar Han and Brown Norway, and wild caught animals, using a combination of manual gene annotation, intact protein mass spectrometry and bottom-up mass spectrometry-based proteomic approaches. Detailed sequencing of the proteins reveals a less complex pattern of primary sequence polymorphism than the mouse. However, unlike the mouse, rat MUPs exhibit added complexity in the form of post-translational modifications including phosphorylation and exoproteolytic trimming of specific isoforms. The possibility that urinary MUPs may have different roles in rat chemical communication than those they play in the house mouse is also discussed.

ACS Style

Guadalupe Gomez-Baena; Stuart D. Armstrong; Josiah O. Halstead; Mark Prescott; Sarah A. Roberts; Lynn McLean; Jonathan M. Mudge; Jane L. Hurst; Robert J. Beynon. Molecular complexity of the major urinary protein system of the Norway rat, Rattus norvegicus. 2018, 478362 .

AMA Style

Guadalupe Gomez-Baena, Stuart D. Armstrong, Josiah O. Halstead, Mark Prescott, Sarah A. Roberts, Lynn McLean, Jonathan M. Mudge, Jane L. Hurst, Robert J. Beynon. Molecular complexity of the major urinary protein system of the Norway rat, Rattus norvegicus. . 2018; ():478362.

Chicago/Turabian Style

Guadalupe Gomez-Baena; Stuart D. Armstrong; Josiah O. Halstead; Mark Prescott; Sarah A. Roberts; Lynn McLean; Jonathan M. Mudge; Jane L. Hurst; Robert J. Beynon. 2018. "Molecular complexity of the major urinary protein system of the Norway rat, Rattus norvegicus." , no. : 478362.

Other
Published: 02 February 2018
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BackgroundTrombidid mites have a unique lifecycle in which only the larval stage is ectoparasitic. In the superfamily Trombiculoidea (“chiggers”), the larvae feed preferentially on vertebrates, including humans. Species in the genusLeptotrombidiumare vectors of a potentially fatal bacterial infection, scrub typhus, which affects 1 million people annually. Moreover, chiggers can cause pruritic dermatitis (trombiculiasis) in humans and domesticated animals. In the Trombidioidea (velvet mites), the larvae feed on other arthropods and are potential biological control agents for agricultural pests. Here, we present the first trombidid mites genomes, obtained both for a chigger,Leptotrombidium deliense, and for a velvet mite,Dinothrombium tinctorium.ResultsSequencing was performed using Illumina technology. A 180 Mb draft assembly forD. tinctoriumwas generated from two paired-end and one mate-pair library using a single adult specimen. ForL. deliense, a lower-coverage draft assembly (117 Mb) was obtained using pooled, engorged larvae with a single paired-end library. Remarkably, both genomes exhibited evidence of ancient lateral gene transfer from soil-derived bacteria or fungi. The transferred genes confer functions that are rare in animals, including terpene and carotenoid synthesis. Thirty-seven allergenic protein families were predicted in theL. deliensegenome, of which nine were unique. Preliminary proteomic analyses identified several of these putative allergens in larvae.ConclusionsTrombidid mite genomes appear to be more dynamic than those of other acariform mites. A priority for future research is to determine the biological function of terpene synthesis in this taxon and its potential for exploitation in disease control.

ACS Style

Xiaofeng Dong; Kittipong Chaisiri; Dong Xia; Stuart D. Armstrong; Yongxiang Fang; Martin J. Donnelly; Tatsuhiko Kadowaki; John W. McGarry; Alistair C. Darby; Benjamin L. Makepeace. Genomes of trombidid mites reveal novel predicted allergens and laterally-transferred genes associated with secondary metabolism. 2018, 259044 .

AMA Style

Xiaofeng Dong, Kittipong Chaisiri, Dong Xia, Stuart D. Armstrong, Yongxiang Fang, Martin J. Donnelly, Tatsuhiko Kadowaki, John W. McGarry, Alistair C. Darby, Benjamin L. Makepeace. Genomes of trombidid mites reveal novel predicted allergens and laterally-transferred genes associated with secondary metabolism. . 2018; ():259044.

Chicago/Turabian Style

Xiaofeng Dong; Kittipong Chaisiri; Dong Xia; Stuart D. Armstrong; Yongxiang Fang; Martin J. Donnelly; Tatsuhiko Kadowaki; John W. McGarry; Alistair C. Darby; Benjamin L. Makepeace. 2018. "Genomes of trombidid mites reveal novel predicted allergens and laterally-transferred genes associated with secondary metabolism." , no. : 259044.

Journal article
Published: 01 November 2015 in International Journal of Mass Spectrometry
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ACS Style

Robert J. Beynon; Stuart D. Armstrong; Amy J. Claydon; Amanda J. Davidson; Claire E. Eyers; James I. Langridge; Guadalupe Gómez-Baena; Victoria M. Harman; Jane L. Hurst; Victoria Lee; Lynn McLean; Rebecca Pattison; Sarah A. Roberts; Deborah M. Simpson; Jenny Unsworth; Matthias Vonderach; Jonathan P. Williams; Yvonne E. Woolerton. Mass spectrometry for structural analysis and quantification of the Major Urinary Proteins of the house mouse. International Journal of Mass Spectrometry 2015, 391, 146 -156.

AMA Style

Robert J. Beynon, Stuart D. Armstrong, Amy J. Claydon, Amanda J. Davidson, Claire E. Eyers, James I. Langridge, Guadalupe Gómez-Baena, Victoria M. Harman, Jane L. Hurst, Victoria Lee, Lynn McLean, Rebecca Pattison, Sarah A. Roberts, Deborah M. Simpson, Jenny Unsworth, Matthias Vonderach, Jonathan P. Williams, Yvonne E. Woolerton. Mass spectrometry for structural analysis and quantification of the Major Urinary Proteins of the house mouse. International Journal of Mass Spectrometry. 2015; 391 ():146-156.

Chicago/Turabian Style

Robert J. Beynon; Stuart D. Armstrong; Amy J. Claydon; Amanda J. Davidson; Claire E. Eyers; James I. Langridge; Guadalupe Gómez-Baena; Victoria M. Harman; Jane L. Hurst; Victoria Lee; Lynn McLean; Rebecca Pattison; Sarah A. Roberts; Deborah M. Simpson; Jenny Unsworth; Matthias Vonderach; Jonathan P. Williams; Yvonne E. Woolerton. 2015. "Mass spectrometry for structural analysis and quantification of the Major Urinary Proteins of the house mouse." International Journal of Mass Spectrometry 391, no. : 146-156.

Book chapter
Published: 10 May 2011 in Advanced Structural Safety Studies
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One strategy to reduce complexity in proteome analysis is through rational reduction of the proteolytic peptides that constitute the analyte for mass spectrometric analysis. Methods for selective isolation of C- and N-terminal peptides have been developed. In this chapter, we outline the context and variety of methods for selective isolation of N-terminal peptides and detail one method based on negative selection through differential removal of internal peptides.

ACS Style

Gemma R. Davidson; Stuart D. Armstrong; Robert J. Beynon. Positional Proteomics at the N-Terminus as a Means of Proteome Simplification. Advanced Structural Safety Studies 2011, 753, 229 -242.

AMA Style

Gemma R. Davidson, Stuart D. Armstrong, Robert J. Beynon. Positional Proteomics at the N-Terminus as a Means of Proteome Simplification. Advanced Structural Safety Studies. 2011; 753 ():229-242.

Chicago/Turabian Style

Gemma R. Davidson; Stuart D. Armstrong; Robert J. Beynon. 2011. "Positional Proteomics at the N-Terminus as a Means of Proteome Simplification." Advanced Structural Safety Studies 753, no. : 229-242.

Journal article
Published: 16 February 2009 in Physiology & Behavior
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Individual variation in a specialised set of scent communication proteins, the major urinary proteins (MUPs), provides a genetic identity signature that underlies individual and kin recognition, and the assessment of heterozygosity in wild house mice. Here we examine the extent to which MUP variation is retained among 30 classical strains of laboratory mice from three main lineages (Castle, C57, Swiss). Normal wild-type variation in urinary MUP pattern appears to have been lost at an early stage in the derivation of the classical laboratory strains. All strains from the Castle and Swiss lineages shared the same “individual” MUP pattern, consistent with common ancestry from very few founders, while those from the C57 lineage shared a different pattern. Notably, individual variation in MUP pattern was no greater within the Swiss outbred ICR (CD-1) strain than typical for inbred strains. Total urinary protein concentration varied considerably between even closely related substrains, together with minor variation in the relative amount of each MUP isoform expressed, although the functional significance of such quantitative variation in MUP expression has yet to be established. Expression was 2–8 fold higher among males, while a MUP expressed by most male but not female wild mice was expressed by C57 males but variably among Castle and Swiss males and occasionally by females in some strains. The lack of normal variation in MUP patterns within and between strains has important implications for the use of laboratory mice in behavioural or neurophysiological research investigating social recognition or mate choice.

ACS Style

Sarah A. Cheetham; Abigail L. Smith; Stuart D. Armstrong; Robert Beynon; Jane L. Hurst. Limited variation in the major urinary proteins of laboratory mice. Physiology & Behavior 2009, 96, 253 -261.

AMA Style

Sarah A. Cheetham, Abigail L. Smith, Stuart D. Armstrong, Robert Beynon, Jane L. Hurst. Limited variation in the major urinary proteins of laboratory mice. Physiology & Behavior. 2009; 96 (2):253-261.

Chicago/Turabian Style

Sarah A. Cheetham; Abigail L. Smith; Stuart D. Armstrong; Robert Beynon; Jane L. Hurst. 2009. "Limited variation in the major urinary proteins of laboratory mice." Physiology & Behavior 96, no. 2: 253-261.

Journal article
Published: 01 January 2008 in Genome Biology
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The major urinary proteins (MUPs) of Mus musculus domesticus are deposited in urine in large quantities, where they bind and release pheromones and also provide an individual 'recognition signal' via their phenotypic polymorphism. Whilst important information about MUP functionality has been gained in recent years, the gene cluster is poorly studied in terms of structure, genic polymorphism and evolution.

ACS Style

Jonathan M Mudge; Stuart D Armstrong; Karen McLaren; Robert J Beynon; Jane L Hurst; Christine Nicholson; Duncan H Robertson; Laurens G Wilming; Jennifer L Harrow. Dynamic instability of the Major Urinary Protein gene family revealed by genomic and phenotypic comparisons between C57 and 129 strain mice. Genome Biology 2008, 9, R91 -R91.

AMA Style

Jonathan M Mudge, Stuart D Armstrong, Karen McLaren, Robert J Beynon, Jane L Hurst, Christine Nicholson, Duncan H Robertson, Laurens G Wilming, Jennifer L Harrow. Dynamic instability of the Major Urinary Protein gene family revealed by genomic and phenotypic comparisons between C57 and 129 strain mice. Genome Biology. 2008; 9 (5):R91-R91.

Chicago/Turabian Style

Jonathan M Mudge; Stuart D Armstrong; Karen McLaren; Robert J Beynon; Jane L Hurst; Christine Nicholson; Duncan H Robertson; Laurens G Wilming; Jennifer L Harrow. 2008. "Dynamic instability of the Major Urinary Protein gene family revealed by genomic and phenotypic comparisons between C57 and 129 strain mice." Genome Biology 9, no. 5: R91-R91.