Salmonella typhimurium mutants generally defective in chemotaxis.

Abstract:

:The mutations of eight chemotaxis-deficient strains of Salmonella typhimurium, including five new mutants in strain LT2, were mapped by P22 transduction in relation to various fla mot deletions in S. abortus-equi. Seven recessive che mutations mapped between motB and flaC: three, all nontumbling, the che region I, adjacent to motB, and four, including one ever-tumbling, in che region II, adjacent to flaC. Mutant che-107, never-tumbling and dominant to wild type, mapped at flaAII, other mutations of which cause either absence of flagella or lack of locomotor function. We surmise that gene flaAII specifies a protein that polymerizes to form an essential component of the basal apparatus (so that absence of gene product prevents formation of flagela); that a component built up from certain mutationally altered proteins cannot transmit (or generate) active rotation of the hook and flagellum, and so causes the Mot (paralysis) phenyotype; and that a component built up from protein with the che-107 alteration permits only counterclockwise rotation, so that the tumble, normally produced by transient clockwise rotation, cannot be effected.

journal_name

J Bacteriol

journal_title

Journal of bacteriology

authors

Collins AL,Stocker BA

doi

10.1128/JB.128.3.754-765.1976

subject

Has Abstract

pub_date

1976-12-01 00:00:00

pages

754-65

issue

3

eissn

0021-9193

issn

1098-5530

journal_volume

128

pub_type

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