## 3 Results
glutamicum_ strains with mutations in the terminator–antiterminator region. The level of gene expression in the strain VB1 (wt) is set to 1. Strains with the mutations G37A, G37A+C77U, and C79U were not tested in this experiment. (**B**) The dependence of the level of valine production on the changes in free energy of the T hairpin. (**C**) The dependence of the level of valine production on the relative level of expression of the _ilvB_ gene in the mutant strains. Data of _ilvB_ expression and valine production are calculated as the average of three experiments. Error bars show standard deviations. of _ilvB_ gene transcription to the control of valine production in _C. glutamicum_ under these cultivation conditions. The levels of _ilvB_ gene expression and valine production also correlated well with the level of AHAS enzyme activity, with r\({}^{2}\) = 0.89 and r\({}^{2}\) = 0.92, respectively, as indicated by a comparison of the data in Figure 4A and in Table 3.  
A significant correlation (r\({}^{2}\) = 0.86, \(p\) < 0.05, Figure 4B) was also observed between the level of valine production of the _ilvBNC_ operon in _C. glutamicum_ mutant strains and the difference in terminator free energy \(\Delta\)\(\Delta\  
transcriptional noise caused by fluctuations in secondary structures should be suppressed. Such an attenuator can be called a \"fast\" attenuator, the functional role and evolutionary origin of which require a separate study. The mutation at position 110 found in the _C. glutamicum_ VF strain obtained by random mutagenesis and selection for valine formation is located at the base of the terminator hairpin within the GGGC tetranucleotide (positions 110-113) complementary to the boundary trinucleotide GCC and is not involved in the formation of the antitermininator hairpin (Figure 3). Since terminal pairs of hairpin nucleotides are usually prone to the decay of complementary bonds, this model suggests that the presence of mutation 110 disrupts the secondary structure of the terminator and contributes to the fact that the boundary GCC trinucleotide escapes into the hairpin structure of the antiterminator, forming complementary bonds with the GGC trinucleotide (positions 36-38). Moreover, this mutation also creates a single-nucleotide spacer between the hairpins in the antitermination state and thus partially blocks the continuous transition to the terminator state. Thus, we believe that although the conserved regulatory region of the _ilvBNC_ operon in _Corynebacterium_ identified by [PERSON] et al. [6] is capable of forming mRNA structures that play the role of a terminator, antiterminator, and antiantitterminator, the role of the latter in transcriptional attenuation is related to two aspects: (a) the transcription pausing that triggers translation and creates conditions for attenuation through the competition between antiterminator and terminator structures, and (b) the conservativity of the leader peptide containing codons of controlling amino acids on which ribosomes pause in case of their deficiency. Contrary to the comparable stability of AAT, AT, and T hairpins, the active interaction of the AAT and AT  
Figure 5: Schematic of attenuator functioning in the _ilvBNC_ operon of _C. glutamicum_. (**A**)—transcriptional pause state, when the upper part of the AAT hairpin (positions 30–52) interacts with RNA polymerase and creates conditions for ribosome landing and translation initiation; (**B**)—state of translational pause, when the ribosome delays the control codons and creates conditions for the formation of the AT hairpin (positions 36–79) and transcription; (**C**)—state of transcriptional termination, when the ribosome quickly passes the control codons, and instead of AT, the T hairpin is formed (positions 77–113), which completes transcription. Denotations: AAT—antiantiterminator; AT—antiterminator; T—terminator; T—unstable terminator when its GCC boundary trinucleotide has bound to form the AT structure.