Fig. 1

The scheme for ppGpp signalling, FA production and ppGpp sensor included in the model. The left colour box illustrates the relationships between ppGpp and growth. ppGpp accumulates at the end of exp. growth phase [6, 8], marked by asterisk. This is described in the model through a depletion of exp. phase-limiting nutrient lim (e.g., main carbohydrate). Increase of ppGpp inhibits the rRNA biosynthesis from P1/P2 promoter [6, 25], which slows down the growth [12]. The termination of growth in stationary (stat) phase was described in the model by the depletion of growth-supporting nutrient nutr (e.g., secondary carbohydrate) (double asterisk). The decrease of ppGpp concentrations in stat phase [6, 8] was described in the model through downregulation of ribosome-mediated synthesis of ppGpp [5]. The right colour box illustrates the relationship between ppGpp and fatty acids. In normal cells Acyl-ACP product of the fatty acid synthesis (FAS) is consumed for membrane PL synthesis (PLS). But in FA-producing cells Acyl-ACP is diverted for the synthesis of FA by thioesterase (Tes) enzyme (orange) [22]. Excessive production of FA leads to Acyl-ACP depletion, which stimulates accumulation of ppGpp [10]. In addition to inhibiting growth, ppGpp inhibits PLS flux (through inhibition of the key enzyme PlsB, [26]), causing transient accumulation of Acyl-ACP, which downregulates FAS flux through a feedback inhibition of key FAS enzymes by Acyl-ACP [20, 26]. FAS and PLS fluxes are also inhibited in stat phase due to decrease in protein synthesis at low rib [22]. The growth is additionally inhibited by PLS decrease [27]. The ppGpp-mediated regulations are shown in blue. The bottom colour box shows the proposed ppGpp-based biosensor. It includes the expression of transcriptional inhibitor I from the P1/P2 promoter and repression of GFP expression by I