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Steven G. Cresawn

Researcher at James Madison University

Publications -  43
Citations -  2406

Steven G. Cresawn is an academic researcher from James Madison University. The author has contributed to research in topics: Genome & Mycobacteriophages. The author has an hindex of 18, co-authored 41 publications receiving 1926 citations. Previous affiliations of Steven G. Cresawn include University of Pittsburgh & University of Florida.

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A Broadly Implementable Research Course in Phage Discovery and Genomics for First-Year Undergraduate Students

TL;DR: A general model in which faculty and teaching assistants from diverse academic institutions are trained to teach a research course for first-year undergraduate students focused on bacteriophage discovery and genomics is developed, showing that this alliance-sourced model not only substantially advances the field of phage genomics but also stimulates students’ interest in science, positively influences academic achievement, and enhances persistence inScience, technology, engineering, and mathematics (STEM) disciplines.
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Phamerator: a bioinformatic tool for comparative bacteriophage genomics

TL;DR: A bioinformatic tool that assorts protein-coding genes into phamilies of related sequences using pairwise comparisons to generate a database of gene relationships, which is used to generate genome maps of multiple phages that incorporate nucleotide and amino acid sequence relationships.
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Whole Genome Comparison of a Large Collection of Mycobacteriophages Reveals a Continuum of Phage Genetic Diversity

TL;DR: To understand the population structure of phages infecting a single host strain, 627 phages of Mycobacterium smegmatis were isolated, sequenced, and compared to reveal a continuum of genetic diversity, albeit with uneven representation of different phages.
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Prophage-mediated defence against viral attack and viral counter-defence.

TL;DR: Characterization of ten Cluster N temperate mycobacteriophages revealed at least five distinct prophage-expressed viral defence systems that interfere with the infection of lytic and temperate phages that are either closely related (homotypic defence) or unrelated (heterotypic Defence) to the prophages.