Role of lipid biosynthesis in the activation of the YycFG signal transduction proteins

LUCÍA PORRINI; GUSTAVO E. SCHUJMAN; DIEGO DE MENDOZA

Tucumán

Congreso; XLV Reunión Anual de la Sociedad Argentina de Investigadores en Bioquímica (SAIB); 2009

Sociedad Argentina de Investigadores en Bioquímica (SAIB)

The YycFG two-component system is the only signal transduction pathway in B. subtilis known to be essential for cell viability. This system is highly conserved in low G+C gram-positive bacteria, including several human pathogens, and regulates important processes such as cell envelope homeostasis, but the signal  modulating its activity is not clearly defined. The YycF response regulator activates the expression of yocH which encodes a putative autolysin. We have previously shown by microarrays analysis that inhibition of fatty acid biosynthesis by cerulenin induces yocH expression. These data pinpointed YycFG as the responsible for the increased yocH expression by responding to the inhibition of lipid biosynthesis. We confirmed this hypothesis analyzing the yocH expression in an yycFG conditional mutant. We found that YycFG depletion in cerulenin-treated cultures avoids yocH overexpression. Inhibition of fatty acid and phospholipid biosynthesis by cerulenin is accompanied by higher intracellular levels of malonyl-CoA and a decrease in fatty acid chain-length in membrane phospholipids. Using mutants in several genes of lipid biosynthesis we found that the activity of YycFG responds to alterations in membrane phospholipid contents. These results provide the first evidence that YycFG signal derivates from membrane lipid homeostasis.