33 research outputs found
Bacillus thuringiensis protoxin: location of toxic border and requirement of non-toxin domain for high-level in vivo production of active toxin
Bacillus thuringiensis protoxin: location of toxic border and requirement of non-toxic domain for high-level in vivo production of active toxin
An ethA mutation in Bacillus subtilis 168 permits induction of sporulation by ethionine and increases DNA modification of bacteriophage phi 105.
In contrast to Escherichia coli and Salmonella typhimurium, Bacillus subtilis could convert ethionine to S-adenosylethionine (SAE), as can Saccharomyces cerevisiae. This conversion was essential for growth inhibition by ethionine because metE mutants which were deficient in S-adenosylmethionine synthetase activity, were resistant to 10 mM ethionine and converted only a small amount of ethionine to SAE. Another mutation (ethA1) produced partial resistance to ethionine (2 mM) and enabled continual sporulation in glucose medium containing 4 mM DL-ethionine. This sporulation induction probably resulted from the effect of SAE, since it was abolished by the addition of a metE1 mutation. The induction of sporulation was not simply controlled by the ratio of SAE to S-adenosylmethionine, but apparently depended on another effect of the ethA1 mutation, which could be demonstrated by comparing the restriction of clear plaque mutants of bacteriophage phi 105 grown in an ethA1 strain with the restriction of those grown in the standard strain. The phages grown in the ethA1 strain showed increased protection against BsuR restriction. We propose that SAE induces sporulation through the inhibition of a key methylation reaction