{"id":{"repo_id":"loma-linda","oai_identifier":"oai:scholarsrepository.llu.edu:etd-2166"},"canonical_url":"https://search.dev.ndltd.org/etd/loma-linda/oai:scholarsrepository.llu.edu:etd-2166","repository":{"repo_id":"loma-linda","name":"Loma Linda University","base_url":"https://scholarsrepository.llu.edu/do/oai/"},"display":{"title":"Isolation and Characterization of a Novel Motility Mutant in SALMONELLA TYPHIMURIUM","abstract":"<p>A new mutant, BT40, isolated from mutagenized cultures of <em>S. typhimurium</em> was deficient in chemotaxis (Che<sup>-</sup> phenotype) in tryptone semisoft agar, but had random motility with a tumbling frequency (37%) similar to that of the parental strain, ST23 (39%). In spatial assays accumulation of BT40 cells in capillary tubes containing attractants was decreased by 33%-59% compared to ST23, but BT40 had a normal response to attractants in temporal assays. The methylation level of the chemotactic proteins was decreased in BT40. At room temperature, the mean swimming speed was 11 μm/s for BT40 and 20 μm/s for ST23; more BT40 cells wobbled (50%) than ST23 cells (30%), also. The proportion of time that the flagella rotated in the clockwise direction was 5% for BT40 and 28% for ST23. Motile BT40 cells had only 1-3 flagella per cell, and the length of the flagellar filaments was only 40% of the normal. The mutant phenotype was designated as CheG<sup>-</sup> and conjugational studies located <em>cheG</em> between 12 min and 33 min on the chromosomal map. Transductional crosses with <em>fla</em> mutants indicated that <em>cheG</em> was located in flagellar region I at 23 min, and complementation analysis with <em>recA fla</em> strains mapped <em>cheG</em> in <em>flaFVIII</em>. Transductional analysis of spontaneous revertants indicated that besides intragenic revertants, there were pseudorevertants with at least 4 types of suppressor mutations: type I suppressors, linked to the class I <em>Tn10</em> by 16%, were located between the <em>Tn10</em> and <em>cheG</em>; type II suppressors, linked to the class I <em>Tn10</em>. by 7%, were distal to <em>cheG</em> with respect to the <em>Tn10</em>; type III were linked to the class I <em>Tn10</em> by 1%; type IV suppressors were not linked to the class I <em>Tn10</em> and included in this type were the suppressor linked by over 60% to the class II <em>Tn10</em>. The CheG<sup>-</sup> phenotype was due to a defect in a flagellar gene that caused the mutant to have short flagella and fewer flagellar filaments resulting in a decrease in the stability of the flagellar bundle. This instability accounted for occurrence of random motility in BT40 even though the individual flagella had a bias to counterclockwise rotation. It is postulated that the <em>cheG</em> mutation prevented normal expression of operons downstream to <em>flaFVIIl</em> in the flagellar regulatory cascade resulting in the pleiotropic defects observed in BT40 cells.</p>","abstract_html":"&lt;p&gt;A new mutant, BT40, isolated from mutagenized cultures of &lt;em&gt;S. typhimurium&lt;/em&gt; was deficient in chemotaxis (Che&lt;sup&gt;-&lt;/sup&gt; phenotype) in tryptone semisoft agar, but had random motility with a tumbling frequency (37%) similar to that of the parental strain, ST23 (39%). In spatial assays accumulation of BT40 cells in capillary tubes containing attractants was decreased by 33%-59% compared to ST23, but BT40 had a normal response to attractants in temporal assays. The methylation level of the chemotactic proteins was decreased in BT40. At room temperature, the mean swimming speed was 11 μm/s for BT40 and 20 μm/s for ST23; more BT40 cells wobbled (50%) than ST23 cells (30%), also. The proportion of time that the flagella rotated in the clockwise direction was 5% for BT40 and 28% for ST23. Motile BT40 cells had only 1-3 flagella per cell, and the length of the flagellar filaments was only 40% of the normal. The mutant phenotype was designated as CheG&lt;sup&gt;-&lt;/sup&gt; and conjugational studies located &lt;em&gt;cheG&lt;/em&gt; between 12 min and 33 min on the chromosomal map. Transductional crosses with &lt;em&gt;fla&lt;/em&gt; mutants indicated that &lt;em&gt;cheG&lt;/em&gt; was located in flagellar region I at 23 min, and complementation analysis with &lt;em&gt;recA fla&lt;/em&gt; strains mapped &lt;em&gt;cheG&lt;/em&gt; in &lt;em&gt;flaFVIII&lt;/em&gt;. Transductional analysis of spontaneous revertants indicated that besides intragenic revertants, there were pseudorevertants with at least 4 types of suppressor mutations: type I suppressors, linked to the class I &lt;em&gt;Tn10&lt;/em&gt; by 16%, were located between the &lt;em&gt;Tn10&lt;/em&gt; and &lt;em&gt;cheG&lt;/em&gt;; type II suppressors, linked to the class I &lt;em&gt;Tn10&lt;/em&gt;. by 7%, were distal to &lt;em&gt;cheG&lt;/em&gt; with respect to the &lt;em&gt;Tn10&lt;/em&gt;; type III were linked to the class I &lt;em&gt;Tn10&lt;/em&gt; by 1%; type IV suppressors were not linked to the class I &lt;em&gt;Tn10&lt;/em&gt; and included in this type were the suppressor linked by over 60% to the class II &lt;em&gt;Tn10&lt;/em&gt;. The CheG&lt;sup&gt;-&lt;/sup&gt; phenotype was due to a defect in a flagellar gene that caused the mutant to have short flagella and fewer flagellar filaments resulting in a decrease in the stability of the flagellar bundle. This instability accounted for occurrence of random motility in BT40 even though the individual flagella had a bias to counterclockwise rotation. It is postulated that the &lt;em&gt;cheG&lt;/em&gt; mutation prevented normal expression of operons downstream to &lt;em&gt;flaFVIIl&lt;/em&gt; in the flagellar regulatory cascade resulting in the pleiotropic defects observed in BT40 cells.&lt;/p&gt;","abstract_has_math":false,"creators":["Chacko, David Matthew"],"institution":null,"degree_name":"Doctor of Philosophy (Medical Science)","degree_level":"Dissertation","degree_discipline":"Biochemistry","degree_department":null,"school":null,"contributors":["Barry L. Taylor","W. Barton Rippon","R. Bruce Wilcox","Anthony Zuccarelli","Jun-ichi Ryu"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":1985,"date_issued":"1985-09-01T07:00:00Z","date_published":"1985-09-01T07:00:00Z","updated_at":"2026-07-24T02:53:44Z","subjects":["Biochemistry","Microbiology","Salmonella typhimurium."],"languages":["English"],"rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarsrepository.llu.edu/etd/1398","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Barry L. Taylor","W. Barton Rippon","R. Bruce Wilcox","Anthony Zuccarelli","Jun-ichi Ryu"]},{"key":"dc:creator","label":"Author","values":["Chacko, David Matthew"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"thesis:degree_discipline","label":"Discipline","values":["Biochemistry"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Doctor of Philosophy (Medical Science)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biochemistry","Microbiology","Salmonella typhimurium."]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["English"]},{"key":"dc:rights","label":"Dc Rights","values":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarsrepository.llu.edu/etd/1398"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["<p>A new mutant, BT40, isolated from mutagenized cultures of <em>S. typhimurium</em> was deficient in chemotaxis (Che<sup>-</sup> phenotype) in tryptone semisoft agar, but had random motility with a tumbling frequency (37%) similar to that of the parental strain, ST23 (39%). In spatial assays accumulation of BT40 cells in capillary tubes containing attractants was decreased by 33%-59% compared to ST23, but BT40 had a normal response to attractants in temporal assays. The methylation level of the chemotactic proteins was decreased in BT40. At room temperature, the mean swimming speed was 11 μm/s for BT40 and 20 μm/s for ST23; more BT40 cells wobbled (50%) than ST23 cells (30%), also. The proportion of time that the flagella rotated in the clockwise direction was 5% for BT40 and 28% for ST23. Motile BT40 cells had only 1-3 flagella per cell, and the length of the flagellar filaments was only 40% of the normal. The mutant phenotype was designated as CheG<sup>-</sup> and conjugational studies located <em>cheG</em> between 12 min and 33 min on the chromosomal map. Transductional crosses with <em>fla</em> mutants indicated that <em>cheG</em> was located in flagellar region I at 23 min, and complementation analysis with <em>recA fla</em> strains mapped <em>cheG</em> in <em>flaFVIII</em>. Transductional analysis of spontaneous revertants indicated that besides intragenic revertants, there were pseudorevertants with at least 4 types of suppressor mutations: type I suppressors, linked to the class I <em>Tn10</em> by 16%, were located between the <em>Tn10</em> and <em>cheG</em>; type II suppressors, linked to the class I <em>Tn10</em>. by 7%, were distal to <em>cheG</em> with respect to the <em>Tn10</em>; type III were linked to the class I <em>Tn10</em> by 1%; type IV suppressors were not linked to the class I <em>Tn10</em> and included in this type were the suppressor linked by over 60% to the class II <em>Tn10</em>. The CheG<sup>-</sup> phenotype was due to a defect in a flagellar gene that caused the mutant to have short flagella and fewer flagellar filaments resulting in a decrease in the stability of the flagellar bundle. This instability accounted for occurrence of random motility in BT40 even though the individual flagella had a bias to counterclockwise rotation. It is postulated that the <em>cheG</em> mutation prevented normal expression of operons downstream to <em>flaFVIIl</em> in the flagellar regulatory cascade resulting in the pleiotropic defects observed in BT40 cells.</p>"]},{"key":"dc:title","label":"Title","values":["Isolation and Characterization of a Novel Motility Mutant in SALMONELLA TYPHIMURIUM"]}]}],"canonical_facts":{"dc:contributor":["Barry L. Taylor","W. Barton Rippon","R. Bruce Wilcox","Anthony Zuccarelli","Jun-ichi Ryu"],"dc:creator":["Chacko, David Matthew"],"dc:description.abstract":["<p>A new mutant, BT40, isolated from mutagenized cultures of <em>S. typhimurium</em> was deficient in chemotaxis (Che<sup>-</sup> phenotype) in tryptone semisoft agar, but had random motility with a tumbling frequency (37%) similar to that of the parental strain, ST23 (39%). In spatial assays accumulation of BT40 cells in capillary tubes containing attractants was decreased by 33%-59% compared to ST23, but BT40 had a normal response to attractants in temporal assays. The methylation level of the chemotactic proteins was decreased in BT40. At room temperature, the mean swimming speed was 11 μm/s for BT40 and 20 μm/s for ST23; more BT40 cells wobbled (50%) than ST23 cells (30%), also. The proportion of time that the flagella rotated in the clockwise direction was 5% for BT40 and 28% for ST23. Motile BT40 cells had only 1-3 flagella per cell, and the length of the flagellar filaments was only 40% of the normal. The mutant phenotype was designated as CheG<sup>-</sup> and conjugational studies located <em>cheG</em> between 12 min and 33 min on the chromosomal map. Transductional crosses with <em>fla</em> mutants indicated that <em>cheG</em> was located in flagellar region I at 23 min, and complementation analysis with <em>recA fla</em> strains mapped <em>cheG</em> in <em>flaFVIII</em>. Transductional analysis of spontaneous revertants indicated that besides intragenic revertants, there were pseudorevertants with at least 4 types of suppressor mutations: type I suppressors, linked to the class I <em>Tn10</em> by 16%, were located between the <em>Tn10</em> and <em>cheG</em>; type II suppressors, linked to the class I <em>Tn10</em>. by 7%, were distal to <em>cheG</em> with respect to the <em>Tn10</em>; type III were linked to the class I <em>Tn10</em> by 1%; type IV suppressors were not linked to the class I <em>Tn10</em> and included in this type were the suppressor linked by over 60% to the class II <em>Tn10</em>. The CheG<sup>-</sup> phenotype was due to a defect in a flagellar gene that caused the mutant to have short flagella and fewer flagellar filaments resulting in a decrease in the stability of the flagellar bundle. This instability accounted for occurrence of random motility in BT40 even though the individual flagella had a bias to counterclockwise rotation. It is postulated that the <em>cheG</em> mutation prevented normal expression of operons downstream to <em>flaFVIIl</em> in the flagellar regulatory cascade resulting in the pleiotropic defects observed in BT40 cells.</p>"],"dc:identifier":["https://scholarsrepository.llu.edu/etd/1398"],"dc:language":["English"],"dc:rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"dc:subject":["Biochemistry","Microbiology","Salmonella typhimurium."],"dc:title":["Isolation and Characterization of a Novel Motility Mutant in SALMONELLA TYPHIMURIUM"],"thesis:degree_discipline":["Biochemistry"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (Medical Science)"]},"updated_at":"2026-07-24T02:53:44Z"}