Fig. 5

A model for synergistic regulation of HSAF biosynthesis by c-di-GMP and 4-HBA via the CdgL-LysR complex formation in L. enzymogenes. a In the presence of nearby fungi, L. enzymogenes appears to be able to stimulate the HSAF (red asterisk) production and secretion to kill them for foods. In this case, the CdgL level was low, unable to significantly activate the transcription of lenB2 (thin black arrow), leading to low 4-HBA production (blue pentagram). It is important to note that the potential activation mechanism remains unknown (question mark). Similarly, the intracellular c-di-GMP (black circle) levels are also likely low, according to our earlier work (Han et al. 2020). In the absence of c-di-GMP or 4-HBA, the CdgL-LysR complex was stable enough to strengthen the binding of LysR to the HSAF operon promoter region, leading to high operon expression (thick red arrow). b In the absence of surrounding fungi or presence of a nutrient-rich signal (lightning symbol), L. enzymogenes could turn off the HSAF biosynthesis to avoid energy waste. At this moment, CdgL likely accumulated via an unknown manner to stimulate the transcription (thick black arrow) of lenB2 to produce higher intracellular levels of 4-HBA. Subsequently, 4-HBA binding to LysR disrupted the LysR-CdgL complex to release CdgL from the LysR-CdgL-DNA ternary complex, resulting in a weak LysR binding to DNA and leading thus to a low HSAF operon expression (thin red arrow). According to our earlier data (Han et al. 2020), the level of c-di-GMP at this moment was high enough to bind with CdgL and to release CdgL from the LysR-CdgL-DNA ternary complex, leading to further decrease the HSAF operon expression