{"id":{"repo_id":"emich","oai_identifier":"oai:commons.emich.edu:theses-1796"},"canonical_url":"https://search.dev.ndltd.org/etd/emich/oai:commons.emich.edu:theses-1796","repository":{"repo_id":"emich","name":"Eastern Michigan University","base_url":"https://commons.emich.edu/do/oai/"},"display":{"title":"Association of <i>glpQ</i> with serum-resistance in <i>salmonella typhimurium</i>","abstract":"<p><em>Salmonella typhimurium</em> is a leading cause of infectious human gastroenteritis and systemic disease when it escapes into the bloodstream. The human serum complement system is central in fighting systemic bacterial infections. <em>S. typhimurium</em> exhibits resistance to killing by complement (serum-resistance), a trait conferred by several known virulence genes. This study investigates a potential chromosomal complement-resistance gene in <em>S. typhimurium</em> tagged by Tn<em>phoA</em> insertional transposon mutagenesis. <em>S. typhimurium</em> strain EM876 has a chromosomal Tn<em>phoA</em> insertion and reduced serum-resistance. Inverse PCR and subsequent DNA sequence analysis reveal the insertion to be in the gene <em>glpQ</em>. <em>glpQ</em> codes for a periplasmic glycerophosphodiester phosphodiesterase involved in glycerol degradation. Complementation assays using a clone of <em>glpQ</em> on a multicopy plasmid are consistent with a role for <em>glpQ</em> in serum-resistance. <em>glpQ</em> is preferentially expressed at 37°C versus 30°C. This is similar to <em>traT</em> and suggests that multiple temperature-regulated genes may contribute to serum-resistance in <em>S. typhimurium</em>.</p>","abstract_html":"&lt;p&gt;&lt;em&gt;Salmonella typhimurium&lt;/em&gt; is a leading cause of infectious human gastroenteritis and systemic disease when it escapes into the bloodstream. The human serum complement system is central in fighting systemic bacterial infections. &lt;em&gt;S. typhimurium&lt;/em&gt; exhibits resistance to killing by complement (serum-resistance), a trait conferred by several known virulence genes. This study investigates a potential chromosomal complement-resistance gene in &lt;em&gt;S. typhimurium&lt;/em&gt; tagged by Tn&lt;em&gt;phoA&lt;/em&gt; insertional transposon mutagenesis. &lt;em&gt;S. typhimurium&lt;/em&gt; strain EM876 has a chromosomal Tn&lt;em&gt;phoA&lt;/em&gt; insertion and reduced serum-resistance. Inverse PCR and subsequent DNA sequence analysis reveal the insertion to be in the gene &lt;em&gt;glpQ&lt;/em&gt;. &lt;em&gt;glpQ&lt;/em&gt; codes for a periplasmic glycerophosphodiester phosphodiesterase involved in glycerol degradation. Complementation assays using a clone of &lt;em&gt;glpQ&lt;/em&gt; on a multicopy plasmid are consistent with a role for &lt;em&gt;glpQ&lt;/em&gt; in serum-resistance. &lt;em&gt;glpQ&lt;/em&gt; is preferentially expressed at 37°C versus 30°C. This is similar to &lt;em&gt;traT&lt;/em&gt; and suggests that multiple temperature-regulated genes may contribute to serum-resistance in &lt;em&gt;S. typhimurium&lt;/em&gt;.&lt;/p&gt;","abstract_has_math":false,"creators":["Mitchell, Kristie Carlotta"],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Open Access Thesis","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["James L. VandenBosch, Phd, Chair","Daniel Clemans, Phd","David Kass, Phd"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-11-15T08:00:00Z","date_published":"2011-11-15T08:00:00Z","updated_at":"2026-07-24T02:16:51Z","subjects":["salmonella","gastroenteristis","serum","qlpQ","Biology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://commons.emich.edu/theses/427","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["James L. VandenBosch, Phd, Chair","Daniel Clemans, Phd","David Kass, Phd"]},{"key":"dc:creator","label":"Author","values":["Mitchell, Kristie Carlotta"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2012-09-24T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Open Access Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["salmonella","gastroenteristis","serum","qlpQ","Biology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://commons.emich.edu/theses/427"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["<p><em>Salmonella typhimurium</em> is a leading cause of infectious human gastroenteritis and systemic disease when it escapes into the bloodstream. The human serum complement system is central in fighting systemic bacterial infections. <em>S. typhimurium</em> exhibits resistance to killing by complement (serum-resistance), a trait conferred by several known virulence genes. This study investigates a potential chromosomal complement-resistance gene in <em>S. typhimurium</em> tagged by Tn<em>phoA</em> insertional transposon mutagenesis. <em>S. typhimurium</em> strain EM876 has a chromosomal Tn<em>phoA</em> insertion and reduced serum-resistance. Inverse PCR and subsequent DNA sequence analysis reveal the insertion to be in the gene <em>glpQ</em>. <em>glpQ</em> codes for a periplasmic glycerophosphodiester phosphodiesterase involved in glycerol degradation. Complementation assays using a clone of <em>glpQ</em> on a multicopy plasmid are consistent with a role for <em>glpQ</em> in serum-resistance. <em>glpQ</em> is preferentially expressed at 37°C versus 30°C. This is similar to <em>traT</em> and suggests that multiple temperature-regulated genes may contribute to serum-resistance in <em>S. typhimurium</em>.</p>"]},{"key":"dc:title","label":"Title","values":["Association of <i>glpQ</i> with serum-resistance in <i>salmonella typhimurium</i>"]}]}],"canonical_facts":{"dc:contributor":["James L. VandenBosch, Phd, Chair","Daniel Clemans, Phd","David Kass, Phd"],"dc:creator":["Mitchell, Kristie Carlotta"],"dc:date.available":["2012-09-24T07:00:00Z"],"dc:description.abstract":["<p><em>Salmonella typhimurium</em> is a leading cause of infectious human gastroenteritis and systemic disease when it escapes into the bloodstream. The human serum complement system is central in fighting systemic bacterial infections. <em>S. typhimurium</em> exhibits resistance to killing by complement (serum-resistance), a trait conferred by several known virulence genes. This study investigates a potential chromosomal complement-resistance gene in <em>S. typhimurium</em> tagged by Tn<em>phoA</em> insertional transposon mutagenesis. <em>S. typhimurium</em> strain EM876 has a chromosomal Tn<em>phoA</em> insertion and reduced serum-resistance. Inverse PCR and subsequent DNA sequence analysis reveal the insertion to be in the gene <em>glpQ</em>. <em>glpQ</em> codes for a periplasmic glycerophosphodiester phosphodiesterase involved in glycerol degradation. Complementation assays using a clone of <em>glpQ</em> on a multicopy plasmid are consistent with a role for <em>glpQ</em> in serum-resistance. <em>glpQ</em> is preferentially expressed at 37°C versus 30°C. This is similar to <em>traT</em> and suggests that multiple temperature-regulated genes may contribute to serum-resistance in <em>S. typhimurium</em>.</p>"],"dc:identifier":["https://commons.emich.edu/theses/427"],"dc:subject":["salmonella","gastroenteristis","serum","qlpQ","Biology"],"dc:title":["Association of <i>glpQ</i> with serum-resistance in <i>salmonella typhimurium</i>"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Open Access Thesis"],"thesis:degree_name":["Master of Science (MS)"]},"updated_at":"2026-07-24T02:16:51Z"}