Deficiency of flagellation in a Bacillus subtilis pleiotropic mutant lacking transketolase.

Abstract

Genetic, biochemical and morphological analysis of flagella formation in gram-negative bacteria, Escherichia coli and Salmonella typhimurium, established an outline of the mechanism of stepwise biogenesis of flagella.1>2) The basal body is joined with the cell surface through several rings.3) In gram-positive bacteria, two ringlike structures also exist.3) The inner ring appears to be in contact with the plasma membrane and the outer ring may be associated with the teichoic acid polymers on the outer surface of the cell.2) Non-flagellate mutants of grampositive bacteria have not been so intensively studied in contrast to gram-negative bacteria. However, Kunst et al.,A) Sekiguchi et al.5) and Ayusawa et al.6) described pleiotropic mutants of Bacillus subtilis, almost all of which were non-motile. All of these mutants seem to be defective in the same unknown component of the cell surface,7) which results in pleiotropic changes such as overproduction of a-amylase and exocellular proteases, and inability of flagella formation. The pap mutant, moreover, was not transformable.8) During the course of studies on isolation and characterization of carbohydrate metabolism mutants of Bacillus, it was found that the transketolase mutation (tkt) in B. subtilis IFO 12114 generated pleiotropic changes; the

Megacell phenotype and its relation to metabolic alterations in transketolase deficient strain of Bacillus pumilus

“…Based on cell envelope analysis, the tkt mutant has been reported to be defective in teichoic acid and teichuronic acid formation (Sasajima and Kumada, 1981b). In the rich media, these cell membrane components may be available from the medium thereby facilitating the normal dynamics of Z-ring formation and cell division process.…”

“…Specifically, the enzymes D-sorbitol permease, D-sorbitol dehydrogenase, glycerol permease, glycerol kinase and glycerol dehydrogenase were insensitive to D-glucose repression (Sasajima and Kumada, 1981a). The authors argue that this may be a result of defective cell-surface structure in the tkt mutant (Sasajima and Kumada, 1981b).…”

“…During growth, tkt deficient Bacillus cells gradually thicken and start to take on a chain-wise configuration, whereas cells of the parent strain remain slender and distinct (Sasajima and Kumada, 1981b). However, details of the morphological plasticity and the potential correlation with metabolic alterations have not been studied for this mutant.…”

Bacillus

“…(cont. ) azotofixans, 8,18,30,32,35,[39][40]8,18,30,32,39,45,48 badius,8,18,30,44,48,50 benzoevorans,8,30,32,38 brevis,8,18,30,33,37,45,48,286,314 antibiotic production,304,305 wall protein,105,231 "caldevelox",40,275 "caldolyticus",10,40,[259][260][261][262][263][264]…”

“…9,15,IS,[32][33][34][35][36][37][38][39][40][41][46][47][48]223. 231,306 insecticidal activity,309 selective medium,41 stearothermophilus,9,18,29,[32][33][34][35][36][37][38][39]44,48,60,77,83,121,[155][156][157]182,226,231,240,[259][260][261][262]266,[271][272]…”