## 5 Approaches to Improve Biofilm-Based Wastewater Treatment
### Enhanced Biofilm Performance by Exploiting SOS  
Another defense mechanism is SOS. It has been intensely studied in the medical field, and it was found that SOS is the main cause of antibiotic resistance by biofilms. SOS is the microbial response system to DNA damage due to the expression of antibiotic resistance genes in bacteria that are in the biofilm [47; 73]. However, SOS has not yet been explored in the context of wastewater treatment. This stress-inducible biofilm has been reported to occur as a result of the induction of SOS when the biofilm experiences stress. SOS is induced as an emergency response to the threat. Chemicals that inhibit microbial growth may induce SOS. When the bacteria are exposed to external stresses, normal cell division is inhibited following DNA damage. The SOS phenomena have been studied in an _E. coli_ biofilm, for which SOS was induced by exposing the biofilm to UV light. When microorganisms growing in biofilms are exposed to a compound that damages DNA, the genes that control SOS are induced by the SOS repressor locus for X-ray sensitivity, involving LexA and sensor/inducer recombinase A (RecA). These DNA repair genes are responsible for repairing damaged DNA [73]. They do this by binding the single-strand DNA to RecA, thereby activating it. This results in the formation of the nucleoprotein filament, which promotes the self-cleavage of LexA, thereby leading to the de-repression of genes responsible for SOS. The helicase unwinds the double-strand DNA, increasing the single-strand DNA. This, in turn, induces an SOS response. This process occurs when a DNA polymerase stalls at a lesion. The first induction of SOS normally involves high-fidelity repair mechanisms, followed by low-fidelity mechanisms; this is because the SOS response is temporally controlled. The several DNA polymerases involved in the damage tolerance pathway, namely PolII (polB), PolIV (dinB), and PolIV (umuC, umuD), are some of the DNA polymerases that remain active even after great DNA damage. They are capable of repairing irreparable DNA lesions that could block DNAreplication. SOS can also be induced by exogenous and endogenous triggers, conjugative plasmid DNA transfer, and transformation [74]. It has been reported that the SOS in _Clostridia_ is induced by methyl methanesulfonate and UV radiation. Moreover, the induction of SOS in _Pseudomonas Aeruginosa_ has been shown to promote biofilm formation [75]. The SOS phenomena can be used to improve the attachment of bacteria. SOS can be exploited to benefit biological wastewater treatment. This can be done via the induction of SOS, such that the microorganism in the biofilm can induce an emergency response to toxic compounds entering WWTPs, thereby inducing their defense mechanism and mitigating the inhibitory effects of toxic compounds on biological processes in WWTPs [47]. It has been noted that the SOS increases the adhesion and is also responsible for the formation of biofilms. Additionally, other studies have reported that SOS is induced by the attachment of bacteria to the surfaces; hence, bacterial adhesion through the flagella increases when SOS occurs [76]. Table 3 compares the effects of different enhancement methods on the biofilm formation. A study conducted by [PERSON] et al. [9] compared silica functionalization (roughness enhancement), dextran functionalization (chemical enhancement), and biofilm pre-seeding (pre-biofilm enhancement) approaches to enhance biofilm formation. The results obtained from this study indicated that the silica functionalization and pre-seeding of carriers with denittirying bacteria improved the rate of NH\({}_{4}\)\({}^{*}\)-N degradation when compared to virgin carriers. Moreover, the dextran-functionalized carrier did not decrease the start-up period. Additionally, [PERSON] et al. [77] showed that the presence of EPS improved the initial attachment of the biofilm. Moreover, [PERSON] et al.