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Genome-wide variation in SARS-CoV-2 reveals evolution and transmission dynamics which are critical considerations for disease control and prevention decisions. Here, we review estimates of the genome-wide viral mutation rates, summarize current COVID-19 case load in the province of Ontario, Canada (5 January 2021), and analyze published SARS-CoV-2 genomes from Ontario (collected prior to 24 November 2020) to test for more infectious genetic variants or lineages.
Calvin P. Sjaarda; Jennifer L. Guthrie; Samira Mubareka; Jared T. Simpson; Bettina Hamelin; Henry Wong; Leanne Mortimer; Robert Slinger; Andrew G. McArthur; Marc Desjardins; Allison McGeer; Tony Mazzulli; Katya Douchant; Danielle Brabant-Kirwan; Ramzi Fattouh; Aaron Campigotto; Samir N. Patel; Nahuel Fittipaldi; Robert I. Colautti; Prameet M. Sheth. Temporal Dynamics and Evolution of SARS-CoV-2 Demonstrate the Necessity of Ongoing Viral Genome Sequencing in Ontario, Canada. mSphere 2021, 6, 1 .
AMA StyleCalvin P. Sjaarda, Jennifer L. Guthrie, Samira Mubareka, Jared T. Simpson, Bettina Hamelin, Henry Wong, Leanne Mortimer, Robert Slinger, Andrew G. McArthur, Marc Desjardins, Allison McGeer, Tony Mazzulli, Katya Douchant, Danielle Brabant-Kirwan, Ramzi Fattouh, Aaron Campigotto, Samir N. Patel, Nahuel Fittipaldi, Robert I. Colautti, Prameet M. Sheth. Temporal Dynamics and Evolution of SARS-CoV-2 Demonstrate the Necessity of Ongoing Viral Genome Sequencing in Ontario, Canada. mSphere. 2021; 6 (3):1.
Chicago/Turabian StyleCalvin P. Sjaarda; Jennifer L. Guthrie; Samira Mubareka; Jared T. Simpson; Bettina Hamelin; Henry Wong; Leanne Mortimer; Robert Slinger; Andrew G. McArthur; Marc Desjardins; Allison McGeer; Tony Mazzulli; Katya Douchant; Danielle Brabant-Kirwan; Ramzi Fattouh; Aaron Campigotto; Samir N. Patel; Nahuel Fittipaldi; Robert I. Colautti; Prameet M. Sheth. 2021. "Temporal Dynamics and Evolution of SARS-CoV-2 Demonstrate the Necessity of Ongoing Viral Genome Sequencing in Ontario, Canada." mSphere 6, no. 3: 1.
Background The aim of this prospective cohort study was to determine the burden of SARS-CoV-2 in air and on surfaces in rooms of patients hospitalized with COVID-19, and to identify patient characteristics associated with SARS-CoV-2 environmental contamination. Methods Nasopharyngeal swabs, surface, and air samples were collected from the rooms of 78 inpatients with COVID-19 at six acute care hospitals in Toronto from March to May 2020. Samples were tested for SARS-CoV-2 viral RNA and cultured to determine potential infectivity. Whole viral genomes were sequenced from nasopharyngeal and surface samples. Association between patient factors and detection of SARS-CoV-2 RNA in surface samples were investigated using a mixed-effects logistic regression model. Findings SARS-CoV-2 RNA was detected from surfaces (125/474 samples; 42/78 patients) and air (3/146 samples; 3/45 patients) in COVID-19 patient rooms; 14% (6/42) of surface samples from three patients yielded viable virus. Viral sequences from nasopharyngeal and surface samples clustered by patient. Multivariable analysis indicated hypoxia at admission, a PCR-positive nasopharyngeal swab with a cycle threshold of ≤30 on or after surface sampling date, higher Charlson co-morbidity score, and shorter time from onset of illness to sample date were significantly associated with detection of SARS-CoV-2 RNA in surface samples. Interpretation The infrequent recovery of infectious SARS-CoV-2 virus from the environment suggests that the risk to healthcare workers from air and near-patient surfaces in acute care hospital wards is likely limited. Surface contamination was greater when patients were earlier in their course of illness and in those with hypoxia, multiple co-morbidities, and higher SARS-CoV-2 RNA concentration in NP swabs. Our results suggest that, while early detection and isolation of COVID-19 patients is important, air and surfaces may pose limited risk a few days after admission to acute care hospitals.
Jonathon D. Kotwa; Alainna J. Jamal; Hamza Mbareche; Lily Yip; Patryk Aftanas; Shiva Barati; Natalie G. Bell; Elizabeth Bryce; Eric D Coomes; Gloria Crowl; Caroline Duchaine; Amna Faheem; Lubna Farooqi; Ryan Hiebert; Kevin Katz; Saman Khan; Robert Kozak; Angel X. Li; Henna P. Mistry; Mohammad Mozafarihashjin; Jalees A. Nasir; Kuganya Nirmalarajah; Emily M. Panousis; Aimee Paterson; Simon Plenderleith; Jeff Powis; Karren Prost; Renee Schryer; Maureen Taylor; Marc Veillette; Titus Wong; Xi Zoe Zhong; Andrew G. McArthur; Allison J. McGeer; Samira Mubareka. Surface and air contamination with SARS-CoV-2 from hospitalized COVID-19 patients in Toronto, Canada. 2021, 1 .
AMA StyleJonathon D. Kotwa, Alainna J. Jamal, Hamza Mbareche, Lily Yip, Patryk Aftanas, Shiva Barati, Natalie G. Bell, Elizabeth Bryce, Eric D Coomes, Gloria Crowl, Caroline Duchaine, Amna Faheem, Lubna Farooqi, Ryan Hiebert, Kevin Katz, Saman Khan, Robert Kozak, Angel X. Li, Henna P. Mistry, Mohammad Mozafarihashjin, Jalees A. Nasir, Kuganya Nirmalarajah, Emily M. Panousis, Aimee Paterson, Simon Plenderleith, Jeff Powis, Karren Prost, Renee Schryer, Maureen Taylor, Marc Veillette, Titus Wong, Xi Zoe Zhong, Andrew G. McArthur, Allison J. McGeer, Samira Mubareka. Surface and air contamination with SARS-CoV-2 from hospitalized COVID-19 patients in Toronto, Canada. . 2021; ():1.
Chicago/Turabian StyleJonathon D. Kotwa; Alainna J. Jamal; Hamza Mbareche; Lily Yip; Patryk Aftanas; Shiva Barati; Natalie G. Bell; Elizabeth Bryce; Eric D Coomes; Gloria Crowl; Caroline Duchaine; Amna Faheem; Lubna Farooqi; Ryan Hiebert; Kevin Katz; Saman Khan; Robert Kozak; Angel X. Li; Henna P. Mistry; Mohammad Mozafarihashjin; Jalees A. Nasir; Kuganya Nirmalarajah; Emily M. Panousis; Aimee Paterson; Simon Plenderleith; Jeff Powis; Karren Prost; Renee Schryer; Maureen Taylor; Marc Veillette; Titus Wong; Xi Zoe Zhong; Andrew G. McArthur; Allison J. McGeer; Samira Mubareka. 2021. "Surface and air contamination with SARS-CoV-2 from hospitalized COVID-19 patients in Toronto, Canada." , no. : 1.
Summary Type I interferons (IFNs) are our first line of defense against virus infection. Recent studies have suggested the ability of SARS-CoV-2 proteins to inhibit IFN responses. Emerging data also suggest that timing and extent of IFN production is associated with manifestation of COVID-19 severity. In spite of progress in understanding how SARS-CoV-2 activates antiviral responses, mechanistic studies into wild-type SARS-CoV-2-mediated induction and inhibition of human type I IFN responses are scarce. Here we demonstrate that SARS-CoV-2 infection induces a type I IFN response in vitro and in moderate cases of COVID-19. In vitro stimulation of type I IFN expression and signaling in human airway epithelial cells is associated with activation of canonical transcriptions factors, and SARS-CoV-2 is unable to inhibit exogenous induction of these responses. Furthermore, we show that physiological levels of IFNα detected in patients with moderate COVID-19 is sufficient to suppress SARS-CoV-2 replication in human airway cells.
Arinjay Banerjee; Nader El-Sayes; Patrick Budylowski; Rajesh Abraham Jacob; Daniel Richard; Hassaan Maan; Jennifer A. Aguiar; Wael L. Demian; Kaushal Baid; Michael R. D'Agostino; Jann Catherine Ang; Tetyana Murdza; Benjamin J.-M. Tremblay; Sam Afkhami; Mehran Karimzadeh; Aaron T. Irving; Lily Yip; Mario Ostrowski; Jeremy A. Hirota; Robert Kozak; Terence D. Capellini; Matthew S. Miller; Bo Wang; Samira Mubareka; Allison J. McGeer; Andrew G. McArthur; Andrew C. Doxey; Karen Mossman. Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses. iScience 2021, 102477 .
AMA StyleArinjay Banerjee, Nader El-Sayes, Patrick Budylowski, Rajesh Abraham Jacob, Daniel Richard, Hassaan Maan, Jennifer A. Aguiar, Wael L. Demian, Kaushal Baid, Michael R. D'Agostino, Jann Catherine Ang, Tetyana Murdza, Benjamin J.-M. Tremblay, Sam Afkhami, Mehran Karimzadeh, Aaron T. Irving, Lily Yip, Mario Ostrowski, Jeremy A. Hirota, Robert Kozak, Terence D. Capellini, Matthew S. Miller, Bo Wang, Samira Mubareka, Allison J. McGeer, Andrew G. McArthur, Andrew C. Doxey, Karen Mossman. Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses. iScience. 2021; ():102477.
Chicago/Turabian StyleArinjay Banerjee; Nader El-Sayes; Patrick Budylowski; Rajesh Abraham Jacob; Daniel Richard; Hassaan Maan; Jennifer A. Aguiar; Wael L. Demian; Kaushal Baid; Michael R. D'Agostino; Jann Catherine Ang; Tetyana Murdza; Benjamin J.-M. Tremblay; Sam Afkhami; Mehran Karimzadeh; Aaron T. Irving; Lily Yip; Mario Ostrowski; Jeremy A. Hirota; Robert Kozak; Terence D. Capellini; Matthew S. Miller; Bo Wang; Samira Mubareka; Allison J. McGeer; Andrew G. McArthur; Andrew C. Doxey; Karen Mossman. 2021. "Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses." iScience , no. : 102477.
Diagnosing antimicrobial resistance (AMR) in the clinic is based on empirical evidence and current gold standard laboratory phenotypic methods. Genotypic methods have the potential advantages of being faster and cheaper, and having improved mechanistic resolution over phenotypic methods. We generated and applied rule-based and logistic regression models to predict the AMR phenotype from Escherichia coli and Pseudomonas aeruginosa multidrug-resistant clinical isolate genomes. By inspecting and evaluating these models, we identified previously unknown β-lactamase substrate activities. In total, 22 unknown β-lactamase substrate activities were experimentally validated using targeted gene expression studies. Our results demonstrate that generating and analysing predictive models can help guide researchers to the mechanisms driving resistance and improve annotation of AMR genes and phenotypic prediction, and suggest that we cannot solely rely on curated knowledge to predict resistance phenotypes.
Kara K. Tsang; Finlay Maguire; Haley L. Zubyk; Sommer Chou; Arman Edalatmand; Gerard D. Wright; Robert G. Beiko; Andrew G. McArthur. Identifying novel β-lactamase substrate activity through in silico prediction of antimicrobial resistance. Microbial Genomics 2021, 7, 000500 .
AMA StyleKara K. Tsang, Finlay Maguire, Haley L. Zubyk, Sommer Chou, Arman Edalatmand, Gerard D. Wright, Robert G. Beiko, Andrew G. McArthur. Identifying novel β-lactamase substrate activity through in silico prediction of antimicrobial resistance. Microbial Genomics. 2021; 7 (1):000500.
Chicago/Turabian StyleKara K. Tsang; Finlay Maguire; Haley L. Zubyk; Sommer Chou; Arman Edalatmand; Gerard D. Wright; Robert G. Beiko; Andrew G. McArthur. 2021. "Identifying novel β-lactamase substrate activity through in silico prediction of antimicrobial resistance." Microbial Genomics 7, no. 1: 000500.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently emerged to cause widespread infections in humans. SARS-CoV-2 infections have been reported in the Kingdom of Saudi Arabia, where Middle East respiratory syndrome coronavirus (MERS-CoV) causes seasonal outbreaks with a case fatality rate of ~37 %. Here we show that there exists a theoretical possibility of future recombination events between SARS-CoV-2 and MERS-CoV RNA. Through computational analyses, we have identified homologous genomic regions within the ORF1ab and S genes that could facilitate recombination, and have analysed co-expression patterns of the cellular receptors for SARS-CoV-2 and MERS-CoV, ACE2 and DPP4, respectively, to identify human anatomical sites that could facilitate co-infection. Furthermore, we have investigated the likely susceptibility of various animal species to MERS-CoV and SARS-CoV-2 infection by comparing known virus spike protein–receptor interacting residues. In conclusion, we suggest that a recombination between SARS-CoV-2 and MERS-CoV RNA is possible and urge public health laboratories in high-risk areas to develop diagnostic capability for the detection of recombined coronaviruses in patient samples.
Arinjay Banerjee; Andrew C. Doxey; Benjamin J.-M. Tremblay; Michael Mansfield; Sonu Subudhi; Jeremy A. Hirota; Matthew S. Miller; Andrew G. McArthur; Samira Mubareka; Karen Mossman. Predicting the recombination potential of severe acute respiratory syndrome coronavirus 2 and Middle East respiratory syndrome coronavirus. Journal of General Virology 2020, 101, 1251 -1260.
AMA StyleArinjay Banerjee, Andrew C. Doxey, Benjamin J.-M. Tremblay, Michael Mansfield, Sonu Subudhi, Jeremy A. Hirota, Matthew S. Miller, Andrew G. McArthur, Samira Mubareka, Karen Mossman. Predicting the recombination potential of severe acute respiratory syndrome coronavirus 2 and Middle East respiratory syndrome coronavirus. Journal of General Virology. 2020; 101 (12):1251-1260.
Chicago/Turabian StyleArinjay Banerjee; Andrew C. Doxey; Benjamin J.-M. Tremblay; Michael Mansfield; Sonu Subudhi; Jeremy A. Hirota; Matthew S. Miller; Andrew G. McArthur; Samira Mubareka; Karen Mossman. 2020. "Predicting the recombination potential of severe acute respiratory syndrome coronavirus 2 and Middle East respiratory syndrome coronavirus." Journal of General Virology 101, no. 12: 1251-1260.
Cancer immunotherapies using monoclonal antibodies to block inhibitory checkpoints are showing durable remissions in many types of cancer patients, although the majority of breast cancer patients acquire little benefit. Human melanoma and lung cancer patient studies suggest that immune checkpoint inhibitors are often potent in patients that already have intratumoral T cell infiltrate; although it remains unknown what types of interventions can result in an intratumoral T cell infiltrate in breast cancer. Using non-T cell-inflamed mammary tumors, we assessed what biological processes and downstream inflammation can overcome the barriers to spontaneous T cell priming. Here we show a specific type of combination therapy, consisting of oncolytic virus and chemotherapy, activates necroptosis and limits tumor growth in autochthonous tumors. Combination therapy activates proinflammatory cytokines; intratumoral influx of myeloid cells and cytotoxic T cell infiltrate in locally treated and distant autochthonous tumors to render them susceptible to immune checkpoint inhibitors.
Samuel T. Workenhe; Andrew Nguyen; David Bakhshinyan; Jiarun Wei; David N. Hare; Kelly L. MacNeill; Yonghong Wan; Andrew Oberst; Jonathan L. Bramson; Jalees A. Nasir; Alyssa Vito; Nader El-Sayes; Sheila K. Singh; Andrew G. McArthur; Karen L. Mossman. De novo necroptosis creates an inflammatory environment mediating tumor susceptibility to immune checkpoint inhibitors. Communications Biology 2020, 3, 645 .
AMA StyleSamuel T. Workenhe, Andrew Nguyen, David Bakhshinyan, Jiarun Wei, David N. Hare, Kelly L. MacNeill, Yonghong Wan, Andrew Oberst, Jonathan L. Bramson, Jalees A. Nasir, Alyssa Vito, Nader El-Sayes, Sheila K. Singh, Andrew G. McArthur, Karen L. Mossman. De novo necroptosis creates an inflammatory environment mediating tumor susceptibility to immune checkpoint inhibitors. Communications Biology. 2020; 3 (1):645.
Chicago/Turabian StyleSamuel T. Workenhe; Andrew Nguyen; David Bakhshinyan; Jiarun Wei; David N. Hare; Kelly L. MacNeill; Yonghong Wan; Andrew Oberst; Jonathan L. Bramson; Jalees A. Nasir; Alyssa Vito; Nader El-Sayes; Sheila K. Singh; Andrew G. McArthur; Karen L. Mossman. 2020. "De novo necroptosis creates an inflammatory environment mediating tumor susceptibility to immune checkpoint inhibitors." Communications Biology 3, no. 1: 645.
Genome sequencing of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is increasingly important to monitor the transmission and adaptive evolution of the virus. The accessibility of high-throughput methods and polymerase chain reaction (PCR) has facilitated a growing ecosystem of protocols. Two differing protocols are tiling multiplex PCR and bait capture enrichment. Each method has advantages and disadvantages but a direct comparison with different viral RNA concentrations has not been performed to assess the performance of these approaches. Here we compare Liverpool amplification, ARTIC amplification, and bait capture using clinical diagnostics samples. All libraries were sequenced using an Illumina MiniSeq with data analyzed using a standardized bioinformatics workflow (SARS-CoV-2 Illumina GeNome Assembly Line; SIGNAL). One sample showed poor SARS-CoV-2 genome coverage and consensus, reflective of low viral RNA concentration. In contrast, the second sample had a higher viral RNA concentration, which yielded good genome coverage and consensus. ARTIC amplification showed the highest depth of coverage results for both samples, suggesting this protocol is effective for low concentrations. Liverpool amplification provided a more even read coverage of the SARS-CoV-2 genome, but at a lower depth of coverage. Bait capture enrichment of SARS-CoV-2 cDNA provided results on par with amplification. While only two clinical samples were examined in this comparative analysis, both the Liverpool and ARTIC amplification methods showed differing efficacy for high and low concentration samples. In addition, amplification-free bait capture enriched sequencing of cDNA is a viable method for generating a SARS-CoV-2 genome sequence and for identification of amplification artifacts.
Jalees A. Nasir; Robert A. Kozak; Patryk Aftanas; Amogelang R. Raphenya; Kendrick M. Smith; Finlay Maguire; Hassaan Maan; Muhannad Alruwaili; Arinjay Banerjee; Hamza Mbareche; Brian P. Alcock; Natalie C. Knox; Karen Mossman; Bo Wang; Julian A. Hiscox; Andrew G. McArthur; Samira Mubareka. A Comparison of Whole Genome Sequencing of SARS-CoV-2 Using Amplicon-Based Sequencing, Random Hexamers, and Bait Capture. Viruses 2020, 12, 895 .
AMA StyleJalees A. Nasir, Robert A. Kozak, Patryk Aftanas, Amogelang R. Raphenya, Kendrick M. Smith, Finlay Maguire, Hassaan Maan, Muhannad Alruwaili, Arinjay Banerjee, Hamza Mbareche, Brian P. Alcock, Natalie C. Knox, Karen Mossman, Bo Wang, Julian A. Hiscox, Andrew G. McArthur, Samira Mubareka. A Comparison of Whole Genome Sequencing of SARS-CoV-2 Using Amplicon-Based Sequencing, Random Hexamers, and Bait Capture. Viruses. 2020; 12 (8):895.
Chicago/Turabian StyleJalees A. Nasir; Robert A. Kozak; Patryk Aftanas; Amogelang R. Raphenya; Kendrick M. Smith; Finlay Maguire; Hassaan Maan; Muhannad Alruwaili; Arinjay Banerjee; Hamza Mbareche; Brian P. Alcock; Natalie C. Knox; Karen Mossman; Bo Wang; Julian A. Hiscox; Andrew G. McArthur; Samira Mubareka. 2020. "A Comparison of Whole Genome Sequencing of SARS-CoV-2 Using Amplicon-Based Sequencing, Random Hexamers, and Bait Capture." Viruses 12, no. 8: 895.
SUMMARY Type I interferons (IFNs) are our first line of defence against a virus. Protein over-expression studies have suggested the ability of SARS-CoV-2 proteins to block IFN responses. Emerging data also suggest that timing and extent of IFN production is associated with manifestation of COVID-19 severity. In spite of progress in understanding how SARS-CoV-2 activates antiviral responses, mechanistic studies into wildtype SARS-CoV-2-mediated induction and inhibition of human type I IFN responses are lacking. Here we demonstrate that SARS-CoV-2 infection induces a mild type I IFN response in vitro and in moderate cases of COVID-19. In vitro stimulation of type I IFN expression and signaling in human airway epithelial cells is associated with activation of canonical transcriptions factors, and SARS-CoV-2 is unable to inhibit exogenous induction of these responses. Our data demonstrate that SARS-CoV-2 is not adept in blocking type I IFN responses and provide support for ongoing IFN clinical trials.
Arinjay Banerjee; Nader El-Sayes; Patrick Budylowski; Daniel Richard; Hassaan Maan; Jennifer A. Aguiar; Kaushal Baid; Michael R. D’Agostino; Jann Catherine Ang; Benjamin J.-M. Tremblay; Sam Afkhami; Mehran Karimzadeh; Aaron T. Irving; Lily Yip; Mario A Ostrowski; Jeremy A. Hirota; Robert Kozak; Terence D. Capellini; Matthew S. Miller; Bo Wang; Samira Mubareka; Allison J. McGeer; Andrew G. McArthur; Andrew C. Doxey; Karen Mossman. Experimental and natural evidence of SARS-CoV-2 infection-induced activation of type I interferon responses. 2020, 1 .
AMA StyleArinjay Banerjee, Nader El-Sayes, Patrick Budylowski, Daniel Richard, Hassaan Maan, Jennifer A. Aguiar, Kaushal Baid, Michael R. D’Agostino, Jann Catherine Ang, Benjamin J.-M. Tremblay, Sam Afkhami, Mehran Karimzadeh, Aaron T. Irving, Lily Yip, Mario A Ostrowski, Jeremy A. Hirota, Robert Kozak, Terence D. Capellini, Matthew S. Miller, Bo Wang, Samira Mubareka, Allison J. McGeer, Andrew G. McArthur, Andrew C. Doxey, Karen Mossman. Experimental and natural evidence of SARS-CoV-2 infection-induced activation of type I interferon responses. . 2020; ():1.
Chicago/Turabian StyleArinjay Banerjee; Nader El-Sayes; Patrick Budylowski; Daniel Richard; Hassaan Maan; Jennifer A. Aguiar; Kaushal Baid; Michael R. D’Agostino; Jann Catherine Ang; Benjamin J.-M. Tremblay; Sam Afkhami; Mehran Karimzadeh; Aaron T. Irving; Lily Yip; Mario A Ostrowski; Jeremy A. Hirota; Robert Kozak; Terence D. Capellini; Matthew S. Miller; Bo Wang; Samira Mubareka; Allison J. McGeer; Andrew G. McArthur; Andrew C. Doxey; Karen Mossman. 2020. "Experimental and natural evidence of SARS-CoV-2 infection-induced activation of type I interferon responses." , no. : 1.
RNA sequencing (RNA-Seq) is a complicated protocol, both in the laboratory in generation of data and at the computer in analysis of results. Several decisions during RNA-Seq library construction have important implications for analysis, most notably strandedness during complementary DNA library construction. Here, we clarify bioinformatic decisions related to strandedness in both alignment of DNA sequencing reads to reference genomes and subsequent determination of transcript abundance.
Krishna A Srinivasan; Suman K Virdee; Andrew G McArthur. Strandedness during cDNA synthesis, the stranded parameter in htseq-count and analysis of RNA-Seq data. Briefings in Functional Genomics 2020, 19, 339 -342.
AMA StyleKrishna A Srinivasan, Suman K Virdee, Andrew G McArthur. Strandedness during cDNA synthesis, the stranded parameter in htseq-count and analysis of RNA-Seq data. Briefings in Functional Genomics. 2020; 19 (5-6):339-342.
Chicago/Turabian StyleKrishna A Srinivasan; Suman K Virdee; Andrew G McArthur. 2020. "Strandedness during cDNA synthesis, the stranded parameter in htseq-count and analysis of RNA-Seq data." Briefings in Functional Genomics 19, no. 5-6: 339-342.
SARS-CoV-2 emerged in December 2019 in Wuhan, China and has since infected over 1.5 million people, of which over 100,000 have died. As SARS-CoV-2 spreads across the planet, speculations remain about the evolution of the virus and the range of human cells that can be infected by SARS-CoV-2. In this study, we report the isolation of SARS-CoV-2 from two COVID-19 patients in Toronto, Canada. We determined the genomic sequences of the two isolates and identified single nucleotide changes in representative populations of our virus stocks. More importantly, we have tested a wide range of human immune cells for infectivity with SARS-CoV-2. We confirm from our studies that human primary peripheral blood mononuclear cells (PBMCs) are not permissive to SARS-CoV-2. As SARS-CoV-2 continues to spread globally, it is essential to monitor any small nucleotide polymorphisms in the virus and to continue to isolate circulating strains of the virus to determine cell susceptibility and pathogenicity using in vitro and in vivo infection models.
Arinjay Banerjee; Jalees A. Nasir; Patrick Budylowski; Lily Yip; Patryk Aftanas; Natasha Christie; Ayoob Ghalami; Kaushal Baid; Amogelang R. Raphenya; Jeremy A Hirota; Matthew S. Miller; Allison J McGeer; Mario A Ostrowski; Robert A. Kozak; Andrew G McArthur; Karen Mossman; Samira Mubareka. Isolation, sequence, infectivity and replication kinetics of SARS-CoV-2. 2020, 1 .
AMA StyleArinjay Banerjee, Jalees A. Nasir, Patrick Budylowski, Lily Yip, Patryk Aftanas, Natasha Christie, Ayoob Ghalami, Kaushal Baid, Amogelang R. Raphenya, Jeremy A Hirota, Matthew S. Miller, Allison J McGeer, Mario A Ostrowski, Robert A. Kozak, Andrew G McArthur, Karen Mossman, Samira Mubareka. Isolation, sequence, infectivity and replication kinetics of SARS-CoV-2. . 2020; ():1.
Chicago/Turabian StyleArinjay Banerjee; Jalees A. Nasir; Patrick Budylowski; Lily Yip; Patryk Aftanas; Natasha Christie; Ayoob Ghalami; Kaushal Baid; Amogelang R. Raphenya; Jeremy A Hirota; Matthew S. Miller; Allison J McGeer; Mario A Ostrowski; Robert A. Kozak; Andrew G McArthur; Karen Mossman; Samira Mubareka. 2020. "Isolation, sequence, infectivity and replication kinetics of SARS-CoV-2." , no. : 1.
SARS-CoV-2 is a novel betacoronavirus and the aetiological agent of the current COVID-19 outbreak that originated in Hubei Province, China. While polymerase chain reaction is the front-line tool for SARS-CoV-2 surveillance, application of amplification-free and culture-free methods for isolation of SARS-CoV-2 RNA, partnered with next-generation sequencing, would provide a useful tool for both surveillance and research of SARS-CoV-2. We here release into the public domain a set of bait capture hybridization probe sequences for enrichment of SARS-CoV-2 RNA from complex biological samples. These probe sequences have been designed using rigorous bioinformatics methods to provide sensitivity, accuracy, and minimal off-target hybridization. Probe design was based on existing, validated approaches for detecting antimicrobial resistance genes in complex samples and it is our hope that this SARS-CoV-2 bait capture platform, once validated by those with samples in hand, will be of aid in combating the current outbreak.
Jalees A. Nasir; David J. Speicher; Robert A. Kozak; Hendrik N. Poinar; Matthew S. Miller; Andrew G. McArthur. Rapid Design of a Bait Capture Platform for Culture- and Amplification-Free Next-Generation Sequencing of SARS-CoV-2. 2020, 1 .
AMA StyleJalees A. Nasir, David J. Speicher, Robert A. Kozak, Hendrik N. Poinar, Matthew S. Miller, Andrew G. McArthur. Rapid Design of a Bait Capture Platform for Culture- and Amplification-Free Next-Generation Sequencing of SARS-CoV-2. . 2020; ():1.
Chicago/Turabian StyleJalees A. Nasir; David J. Speicher; Robert A. Kozak; Hendrik N. Poinar; Matthew S. Miller; Andrew G. McArthur. 2020. "Rapid Design of a Bait Capture Platform for Culture- and Amplification-Free Next-Generation Sequencing of SARS-CoV-2." , no. : 1.
Purpose Antimicrobial resistance (AMR), especially multidrug resistance, is one of the most serious global threats facing public health. We performed a proof of concept study assessing the suitability of shotgun proteomics as a complementary approach to whole‐genome sequencing (WGS) for detecting AMR determinants. Experimental design We used previously published shotgun proteomics and WGS data on four isolates of Campylobacter jejuni to perform AMR detection by searching the Comprehensive Antibiotic Resistance Database, and we assessed their detection ability relative to genomics screening and traditional phenotypic testing measured by minimum inhibitory concentration. Results Both genomic and proteomic approaches identified the wild type and variant molecular determinants responsible for resistance to tetracycline and ciprofloxacin, in agreement with phenotypic testing. In contrast, the genomic method identified the presence of the β‐lactamase gene, blaOXA‐61, in three isolates. However, its corresponding protein product was detected in only a single isolate, consistent with results obtained from phenotypic testing. This article is protected by copyright. All rights reserved
Chih‐Yu Chen; Clifford G. Clark; Stacie Langner; David Boyd; Amrita Bharat; Stuart J. McCorrister; Andrew McArthur; Morag R. Graham; Garrett R. Westmacott; Gary Van Domselaar. Detection of Antimicrobial Resistance Using Proteomics and the Comprehensive Antibiotic Resistance Database: A Case Study. PROTEOMICS – Clinical Applications 2019, 14, e1800182 .
AMA StyleChih‐Yu Chen, Clifford G. Clark, Stacie Langner, David Boyd, Amrita Bharat, Stuart J. McCorrister, Andrew McArthur, Morag R. Graham, Garrett R. Westmacott, Gary Van Domselaar. Detection of Antimicrobial Resistance Using Proteomics and the Comprehensive Antibiotic Resistance Database: A Case Study. PROTEOMICS – Clinical Applications. 2019; 14 (4):e1800182.
Chicago/Turabian StyleChih‐Yu Chen; Clifford G. Clark; Stacie Langner; David Boyd; Amrita Bharat; Stuart J. McCorrister; Andrew McArthur; Morag R. Graham; Garrett R. Westmacott; Gary Van Domselaar. 2019. "Detection of Antimicrobial Resistance Using Proteomics and the Comprehensive Antibiotic Resistance Database: A Case Study." PROTEOMICS – Clinical Applications 14, no. 4: e1800182.
Identification of the nucleotide sequences encoding antibiotic resistance elements and determination of their association with antibiotic resistance are critical to improve surveillance and monitor trends in antibiotic resistance. Current methods to study antibiotic resistance in various environments rely on extensive deep sequencing or laborious culturing of fastidious organisms, both of which are heavily time-consuming operations.
Allison K. Guitor; Amogelang R. Raphenya; Jennifer Klunk; Melanie Kuch; Brian Alcock; Michael G. Surette; Andrew G. McArthur; Hendrik N. Poinar; Gerard D. Wright. Capturing the Resistome: a Targeted Capture Method To Reveal Antibiotic Resistance Determinants in Metagenomes. Antimicrobial Agents and Chemotherapy 2019, 64, 1 .
AMA StyleAllison K. Guitor, Amogelang R. Raphenya, Jennifer Klunk, Melanie Kuch, Brian Alcock, Michael G. Surette, Andrew G. McArthur, Hendrik N. Poinar, Gerard D. Wright. Capturing the Resistome: a Targeted Capture Method To Reveal Antibiotic Resistance Determinants in Metagenomes. Antimicrobial Agents and Chemotherapy. 2019; 64 (1):1.
Chicago/Turabian StyleAllison K. Guitor; Amogelang R. Raphenya; Jennifer Klunk; Melanie Kuch; Brian Alcock; Michael G. Surette; Andrew G. McArthur; Hendrik N. Poinar; Gerard D. Wright. 2019. "Capturing the Resistome: a Targeted Capture Method To Reveal Antibiotic Resistance Determinants in Metagenomes." Antimicrobial Agents and Chemotherapy 64, no. 1: 1.
Bacteria have evolved sophisticated mechanisms to inhibit the growth of competitors1. One such mechanism involves type VI secretion systems, which bacteria can use to inject antibacterial toxins directly into neighbouring cells. Many of these toxins target the integrity of the cell envelope, but the full range of growth inhibitory mechanisms remains unknown2. Here we identify a type VI secretion effector, Tas1, in the opportunistic pathogen Pseudomonas aeruginosa. The crystal structure of Tas1 shows that it is similar to enzymes that synthesize (p)ppGpp, a broadly conserved signalling molecule in bacteria that modulates cell growth rate, particularly in response to nutritional stress3. However, Tas1 does not synthesize (p)ppGpp; instead, it pyrophosphorylates adenosine nucleotides to produce (p)ppApp at rates of nearly 180,000 molecules per minute. Consequently, the delivery of Tas1 into competitor cells drives rapid accumulation of (p)ppApp, depletion of ATP, and widespread dysregulation of essential metabolic pathways, thereby resulting in target cell death. Our findings reveal a previously undescribed mechanism for interbacterial antagonism and demonstrate a physiological role for the metabolite (p)ppApp in bacteria. The bacterium Pseudomonas aeruginosa attacks competing bacteria using the toxin Tas1, which pyrophosphorylates adenosine nucleotides to generate (p)ppApp, thereby depleting ATP and disrupting multiple cellular functions.
Shehryar Ahmad; Boyuan Wang; Matthew D. Walker; Hiu-Ki R. Tran; Peter J. Stogios; Alexei Savchenko; Robert A. Grant; Andrew McArthur; Michael T. Laub; John C. Whitney. An interbacterial toxin inhibits target cell growth by synthesizing (p)ppApp. Nature 2019, 575, 674 -678.
AMA StyleShehryar Ahmad, Boyuan Wang, Matthew D. Walker, Hiu-Ki R. Tran, Peter J. Stogios, Alexei Savchenko, Robert A. Grant, Andrew McArthur, Michael T. Laub, John C. Whitney. An interbacterial toxin inhibits target cell growth by synthesizing (p)ppApp. Nature. 2019; 575 (7784):674-678.
Chicago/Turabian StyleShehryar Ahmad; Boyuan Wang; Matthew D. Walker; Hiu-Ki R. Tran; Peter J. Stogios; Alexei Savchenko; Robert A. Grant; Andrew McArthur; Michael T. Laub; John C. Whitney. 2019. "An interbacterial toxin inhibits target cell growth by synthesizing (p)ppApp." Nature 575, no. 7784: 674-678.
The Comprehensive Antibiotic Resistance Database (CARD; https://card.mcmaster.ca) is a curated resource providing reference DNA and protein sequences, detection models and bioinformatics tools on the molecular basis of bacterial antimicrobial resistance (AMR). CARD focuses on providing high-quality reference data and molecular sequences within a controlled vocabulary, the Antibiotic Resistance Ontology (ARO), designed by the CARD biocuration team to integrate with software development efforts for resistome analysis and prediction, such as CARD’s Resistance Gene Identifier (RGI) software. Since 2017, CARD has expanded through extensive curation of reference sequences, revision of the ontological structure, curation of over 500 new AMR detection models, development of a new classification paradigm and expansion of analytical tools. Most notably, a new Resistomes & Variants module provides analysis and statistical summary of in silico predicted resistance variants from 82 pathogens and over 100 000 genomes. By adding these resistance variants to CARD, we are able to summarize predicted resistance using the information included in CARD, identify trends in AMR mobility and determine previously undescribed and novel resistance variants. Here, we describe updates and recent expansions to CARD and its biocuration process, including new resources for community biocuration of AMR molecular reference data.
Brian P Alcock; Amogelang R Raphenya; Tammy T Y Lau; Kara K Tsang; Mégane Bouchard; Arman Edalatmand; William Huynh; Anna-Lisa V Nguyen; Annie A Cheng; Sihan Liu; Sally Y Min; Anatoly Miroshnichenko; Hiu-Ki Tran; Rafik E Werfalli; Jalees A Nasir; Martins Oloni; David J Speicher; Alexandra Florescu; Bhavya Singh; Mateusz Faltyn; Anastasia Hernandez-Koutoucheva; Arjun N Sharma; Emily Bordeleau; Andrew C Pawlowski; Haley L Zubyk; Damion Dooley; Emma Griffiths; Finlay Maguire; Geoff L Winsor; Robert G Beiko; Fiona S L Brinkman; William W L Hsiao; Gary V Domselaar; Andrew G McArthur. CARD 2020: antibiotic resistome surveillance with the comprehensive antibiotic resistance database. Nucleic Acids Research 2019, 48, D517 -D525.
AMA StyleBrian P Alcock, Amogelang R Raphenya, Tammy T Y Lau, Kara K Tsang, Mégane Bouchard, Arman Edalatmand, William Huynh, Anna-Lisa V Nguyen, Annie A Cheng, Sihan Liu, Sally Y Min, Anatoly Miroshnichenko, Hiu-Ki Tran, Rafik E Werfalli, Jalees A Nasir, Martins Oloni, David J Speicher, Alexandra Florescu, Bhavya Singh, Mateusz Faltyn, Anastasia Hernandez-Koutoucheva, Arjun N Sharma, Emily Bordeleau, Andrew C Pawlowski, Haley L Zubyk, Damion Dooley, Emma Griffiths, Finlay Maguire, Geoff L Winsor, Robert G Beiko, Fiona S L Brinkman, William W L Hsiao, Gary V Domselaar, Andrew G McArthur. CARD 2020: antibiotic resistome surveillance with the comprehensive antibiotic resistance database. Nucleic Acids Research. 2019; 48 ():D517-D525.
Chicago/Turabian StyleBrian P Alcock; Amogelang R Raphenya; Tammy T Y Lau; Kara K Tsang; Mégane Bouchard; Arman Edalatmand; William Huynh; Anna-Lisa V Nguyen; Annie A Cheng; Sihan Liu; Sally Y Min; Anatoly Miroshnichenko; Hiu-Ki Tran; Rafik E Werfalli; Jalees A Nasir; Martins Oloni; David J Speicher; Alexandra Florescu; Bhavya Singh; Mateusz Faltyn; Anastasia Hernandez-Koutoucheva; Arjun N Sharma; Emily Bordeleau; Andrew C Pawlowski; Haley L Zubyk; Damion Dooley; Emma Griffiths; Finlay Maguire; Geoff L Winsor; Robert G Beiko; Fiona S L Brinkman; William W L Hsiao; Gary V Domselaar; Andrew G McArthur. 2019. "CARD 2020: antibiotic resistome surveillance with the comprehensive antibiotic resistance database." Nucleic Acids Research 48, no. : D517-D525.
Glycopeptide antibiotics are produced by Actinobacteria through biosynthetic gene clusters that include genes supporting their regulation, synthesis, export and resistance. The chemical and biosynthetic diversities of glycopeptides are the product of an intricate evolutionary history. Extracting this history from genome sequences is difficult as conservation of the individual components of these gene clusters is variable and each component can have a different trajectory. We show that glycopeptide biosynthesis and resistance in Actinobacteria maps to approximately 150-400 million years ago. Phylogenetic reconciliation reveals that the precursors of glycopeptide biosynthesis are far older than other components, implying that these clusters arose from a pre-existing pool of genes. We find that resistance appeared contemporaneously with biosynthetic genes, raising the possibility that the mechanism of action of glycopeptides was a driver of diversification in these gene clusters. Our results put antibiotic biosynthesis and resistance into an evolutionary context and can guide the future discovery of compounds possessing new mechanisms of action, which are especially needed as the usefulness of the antibiotics available at present is imperilled by human activity.
Nicholas Waglechner; Andrew McArthur; Gerard D. Wright. Phylogenetic reconciliation reveals the natural history of glycopeptide antibiotic biosynthesis and resistance. Nature Microbiology 2019, 4, 1862 -1871.
AMA StyleNicholas Waglechner, Andrew McArthur, Gerard D. Wright. Phylogenetic reconciliation reveals the natural history of glycopeptide antibiotic biosynthesis and resistance. Nature Microbiology. 2019; 4 (11):1862-1871.
Chicago/Turabian StyleNicholas Waglechner; Andrew McArthur; Gerard D. Wright. 2019. "Phylogenetic reconciliation reveals the natural history of glycopeptide antibiotic biosynthesis and resistance." Nature Microbiology 4, no. 11: 1862-1871.
RNA sequencing (RNA-Seq) is a complicated protocol, both in the laboratory in generation of data and at the computer in analysis of results. Several decisions during RNA-Seq library construction have important implications for analysis, most notably strandedness during complementary DNA (cDNA) library construction. Here we clarify bioinformatic decisions related to strandedness in both alignment of DNA sequencing reads to reference genomes and subsequent determination of transcript abundance.
Krishna Srinivasan; Suman Virdee; Andrew McArthur. Strandedness During cDNA Synthesis, the Stranded Parameter in htseq-count, and Analysis of RNA-Seq Data. 2019, 1 .
AMA StyleKrishna Srinivasan, Suman Virdee, Andrew McArthur. Strandedness During cDNA Synthesis, the Stranded Parameter in htseq-count, and Analysis of RNA-Seq Data. . 2019; ():1.
Chicago/Turabian StyleKrishna Srinivasan; Suman Virdee; Andrew McArthur. 2019. "Strandedness During cDNA Synthesis, the Stranded Parameter in htseq-count, and Analysis of RNA-Seq Data." , no. : 1.
Whole genome sequencing (WGS) is a powerful tool for public health infectious disease investigations owing to its higher resolution, greater efficiency, and cost-effectiveness over traditional genotyping methods. Implementation of WGS in routine public health microbiology laboratories is impeded by a lack of user-friendly automated and semi-automated pipelines, restrictive jurisdictional data sharing policies, and the proliferation of non-interoperable analytical and reporting systems. To address these issues, we developed the Integrated Rapid Infectious Disease Analysis (IRIDA) platform (irida.ca), a user-friendly, decentralized, open-source bioinformatics and analytical web platform to support real-time infectious disease outbreak investigations using WGS data. Instances can be independently installed on local high-performance computing infrastructure, enabling private and secure data management and analyses according to organizational policies and governance. IRIDA’s data management capabilities enable secure upload, storage and sharing of all WGS data and metadata. The core platform currently includes pipelines for quality control, assembly, annotation, variant detection, phylogenetic analysis, in silico serotyping, multi-locus sequence typing, and genome distance calculation. Analysis pipeline results can be visualized within the platform through dynamic line lists and integrated phylogenomic clustering for research and discovery, and for enhancing decision-making support and hypothesis generation in epidemiological investigations. Communication and data exchange between instances are provided through customizable access controls. IRIDA complements centralized systems, empowering local analytics and visualizations for genomics-based microbial pathogen investigations. IRIDA is currently transforming the Canadian public health ecosystem and is freely available at https://github.com/phac-nml/irida and www.irida.ca.Impact StatementWhole genome sequencing (WGS) is revolutionizing infectious disease analysis and surveillance due to its cost effectiveness, utility, and improved analytical power. To date, no “one-size-fits-all” genomics platform has been universally adopted, owing to differences in national (and regional) health information systems, data sharing policies, computational infrastructures, lack of interoperability and prohibitive costs. The Integrated Rapid Infectious Disease Analysis (IRIDA) platform is a user-friendly, decentralized, open-source bioinformatics and analytical web platform developed to support real-time infectious disease outbreak investigations using WGS data. IRIDA empowers public health, regulatory and clinical microbiology laboratory personnel to better incorporate WGS technology into routine operations by shielding them from the computational and analytical complexities of big data genomics. IRIDA is now routinely used as part of a validated suite of tools to support outbreak investigations in Canada....
Thomas C Matthews; Franklin R Bristow; Emma J Griffiths; Aaron Petkau; Josh Adam; Damion Dooley; Peter Kruczkiewicz; John Curatcha; Jennifer Cabral; Dan Fornika; Geoffrey L. Winsor; Melanie Courtot; Claire Bertelli; Ataollah Roudgar; Pedro Feijao; Philip Mabon; Eric Enns; Joel Thiessen; Alexander Keddy; Judith Isaac-Renton; Jennifer L. Gardy; Patrick Tang; The IRIDA Consortium João A Carriço; Leonid Chindelevitch; Cedric Chauve; Morag R Graham; Andrew G McArthur; Eduardo N Taboada; Robert G Beiko; Fiona Sl Brinkman; William Wl Hsiao; Gary Van Domselaar; Joao A Carrico; The IRIDA Consortium. The Integrated Rapid Infectious Disease Analysis (IRIDA) Platform. 2018, 381830 .
AMA StyleThomas C Matthews, Franklin R Bristow, Emma J Griffiths, Aaron Petkau, Josh Adam, Damion Dooley, Peter Kruczkiewicz, John Curatcha, Jennifer Cabral, Dan Fornika, Geoffrey L. Winsor, Melanie Courtot, Claire Bertelli, Ataollah Roudgar, Pedro Feijao, Philip Mabon, Eric Enns, Joel Thiessen, Alexander Keddy, Judith Isaac-Renton, Jennifer L. Gardy, Patrick Tang, The IRIDA Consortium João A Carriço, Leonid Chindelevitch, Cedric Chauve, Morag R Graham, Andrew G McArthur, Eduardo N Taboada, Robert G Beiko, Fiona Sl Brinkman, William Wl Hsiao, Gary Van Domselaar, Joao A Carrico, The IRIDA Consortium. The Integrated Rapid Infectious Disease Analysis (IRIDA) Platform. . 2018; ():381830.
Chicago/Turabian StyleThomas C Matthews; Franklin R Bristow; Emma J Griffiths; Aaron Petkau; Josh Adam; Damion Dooley; Peter Kruczkiewicz; John Curatcha; Jennifer Cabral; Dan Fornika; Geoffrey L. Winsor; Melanie Courtot; Claire Bertelli; Ataollah Roudgar; Pedro Feijao; Philip Mabon; Eric Enns; Joel Thiessen; Alexander Keddy; Judith Isaac-Renton; Jennifer L. Gardy; Patrick Tang; The IRIDA Consortium João A Carriço; Leonid Chindelevitch; Cedric Chauve; Morag R Graham; Andrew G McArthur; Eduardo N Taboada; Robert G Beiko; Fiona Sl Brinkman; William Wl Hsiao; Gary Van Domselaar; Joao A Carrico; The IRIDA Consortium. 2018. "The Integrated Rapid Infectious Disease Analysis (IRIDA) Platform." , no. : 381830.
Introduction Prokaryotic microorganisms were the only form of life for at least 80 percent of our evolutionary history (Schopf and Packer, 1987). Multicellular organisms including plants, animals and fungi evolved a mere 0.5–1.0 Ga from single-celled eukaryotic ancestors. Geologists and paleontologists debate the age of life on this planet and when the major microbial lineages first diverged (see Chapter 12 for details). Cyanobacterium-like fossils suggest that life emerged at least 3.45 Ga (Schopf et al., 2002; Schopf and Packer, 1987), but the biogenic origins of these structures are contested (Brasier et al., 2002; Section 12.2.1). The chemical record documents prokaryotic metabolisms that may have existed 3.47–3.85 Ga (Mojzsis et al., 1996) and eukaryotic biosignatures that may be as old as 2.7 Gyr (Brocks et al., 1999). Yet, these are still imprecise interpretations (some might be more recent microbial contamination) and do not set absolute limits on the possible origins of life on Earth. Early periods of heavy bombardment between 4.1 and 3.8 Ga might constrain when life first appeared on Earth, although microorganisms living off chemical energy at kilometer depths could have survived even the largest impact events. By the standards of multicellular plants and animals, single-cell organisms look relatively simple (Patterson and Sogin, 1993), yet they transformed the atmosphere, the waters, the surface, and the subsurface of the Earth.
Mitchell L. Sogin; David J. Patterson; Andrew McArthur; Iii Woodruff T. Sullivan; John Baross. The origin and diversification of eukaryotes. Planets and Life 2018, 265 -274.
AMA StyleMitchell L. Sogin, David J. Patterson, Andrew McArthur, Iii Woodruff T. Sullivan, John Baross. The origin and diversification of eukaryotes. Planets and Life. 2018; ():265-274.
Chicago/Turabian StyleMitchell L. Sogin; David J. Patterson; Andrew McArthur; Iii Woodruff T. Sullivan; John Baross. 2018. "The origin and diversification of eukaryotes." Planets and Life , no. : 265-274.
Round whitefish (Prosopium cylindraceum) have a broad, disjunct range across northern North America and Eurasia, and little is known about their genetic population structure. We performed genetic analyses of round whitefish from 17 sites across its range using nine microsatellites, two mitochondrial DNA (mtDNA) loci, and 4918 to 8835 single-nucleotide polymorphism (SNP) loci. Our analyses identified deep phylogenetic division between eastern and western portions of the range, likely indicative of origins from at least two separate Pleistocene glacial refugia. Regionally, microsatellites and SNPs identified congruent patterns in subdivision, and population structure was consistent with expectations based on hydrologic connectivity. Within the Laurentian Great Lakes, Lake Huron and Lake Ontario were identified as key areas of interest. Lake Huron appears to be a contemporary source population for several other Great Lakes, and Lake Ontario contains a genetically discrete group of round whitefish. In all cases, multiple genetic markers yielded similar patterns, but SNPs offered substantially enhanced resolution. We conclude that round whitefish have population subdivision on several scales important for understanding their evolutionary history and conservation planning.
Thomas D. Morgan; Carly F. Graham; Andrew G. McArthur; Amogelang R. Raphenya; Douglas R. Boreham; Richard G. Manzon; Joanna Y. Wilson; Stacey L. Lance; Kimberly L. Howland; Paul H. Patrick; Christopher M. Somers; Master of Science. Genetic population structure of the round whitefish (Prosopium cylindraceum) in North America: multiple markers reveal glacial refugia and regional subdivision. Canadian Journal of Fisheries and Aquatic Sciences 2018, 75, 836 -849.
AMA StyleThomas D. Morgan, Carly F. Graham, Andrew G. McArthur, Amogelang R. Raphenya, Douglas R. Boreham, Richard G. Manzon, Joanna Y. Wilson, Stacey L. Lance, Kimberly L. Howland, Paul H. Patrick, Christopher M. Somers, Master of Science. Genetic population structure of the round whitefish (Prosopium cylindraceum) in North America: multiple markers reveal glacial refugia and regional subdivision. Canadian Journal of Fisheries and Aquatic Sciences. 2018; 75 (6):836-849.
Chicago/Turabian StyleThomas D. Morgan; Carly F. Graham; Andrew G. McArthur; Amogelang R. Raphenya; Douglas R. Boreham; Richard G. Manzon; Joanna Y. Wilson; Stacey L. Lance; Kimberly L. Howland; Paul H. Patrick; Christopher M. Somers; Master of Science. 2018. "Genetic population structure of the round whitefish (Prosopium cylindraceum) in North America: multiple markers reveal glacial refugia and regional subdivision." Canadian Journal of Fisheries and Aquatic Sciences 75, no. 6: 836-849.