Induction of morphogenesis by methionine starvation in Myxococcus xanthus: polyamine control. Academic Article uri icon

Overview

MeSH Major

  • Amines
  • Bacteria
  • Methionine

abstract

  • The induction of mycrocyst formation by methionine starvation was demonstrated in Myxococcus xanthus by several methods. Growing in a defined medium (M(1)), M. xanthus had a doubling time of 6.5 hr. Four amino acids-leucine, isoleucine, valine, and glycine-were required for growth under these conditions. When the concentration of several amino acids in the medium was reduced (M(2)), the doubling time increased to 10 to 12 hr, and a requirement for methionine was observed. Methionine starvation led to a slow conversion of the population to microcysts. Under conditions of methionine prototrophy (M(1)), microcyst formation could still be triggered in exponentially growing cells by the addition of either 5 mm ethionine or 0.1 m isoleucine plus 0.1 m threonine, feedback inhibitors of methionine biosynthesis. Vegetative growth in the absence of methionine was obtained in medium M(2) if the leucine concentration was raised to its level in medium M(1). Thus, methionine biosynthesis is controlled by the exogenous concentration of the required amino acid, leucine. During an examination of the effects of methionine metabolites on microcyst formation, the involvement of polyamines in morphogenesis was uncovered. Putrescine (0.05 m) induced the formation of microcysts; spermidine (2 to 5 mm) inhibited induction by methionine starvation, ethionine, or high isoleucine-threonine. Spermidine was the only polyamine detected in M. xanthus (16.0 mug/10(9) cells). Its concentration decreased by more than 50% shortly after microcyst induction by high isoleucine-threonine. It is postulated that spermidine is an inhibitor of microcyst induction; when spermidine formation is blocked by methionine starvation, morphogenesis is induced.

publication date

  • September 1970

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC248138

PubMed ID

  • 4097531

Additional Document Info

start page

  • 641

end page

  • 9

volume

  • 103

number

  • 3