Physical and chemical microenvironments within the biofilm (e.g., varied conditions of pH, osmotic strength, nutrients or exposure to sublethal concentrations of biocide) induce heterogeneous metabolic activity and adaptive responses among biofilm cells (Bridier et al., 2011; Giaouris et al., 2015). During biofilm development, the population displays multiple phenotypes (Sauer et al., 2002). At the single cell scale, the diversity of cell properties are due to either the phenotypic adaptation driven by up- or down- regulation of gene expression, or the appearance of genetic mutants driven by an increased level of mutation in biofilm environment.

Gene regulation at different stages of biofilm formation, compared to the free-living mode of life, can be studied through the comparison of transcriptomic (Waite et al., 2006; Moreno-Paz et al., 2010; Guilhen et al., 2016), proteomic (Sauer, 2003; Resch et al., 2006; Vilain and Brozel, 2006; Giaouris et al., 2013; Qayyum et al., 2016) or metabolomic (Wong et al., 2015; Stipetic et al., 2016) profiles revealing up- or down- regulated functions. For example, in mature biofilms of P. aeruginosa, more than 50% of proteins are upregulated and more than 100 proteins are de novo synthesized in comparison to planktonic cells (Sauer et al., 2002). The multiple phenotypes described in biofilm communities do not correspond to a simple mixture of planktonic cells at different growth stages. The biofilm proteome of Bacillus cereus was for example demonstrated as unique and different from those of exponential and stationary-phase planktonic cells (Vilain and Brozel, 2006). Compared lipidomics between planktonic and biofilm cells also support the idea of specific biofilm phenotypes. Indeed, in various growth conditions, the biofilm cell membrane of different bacterial strains was shown to be more saturated than their planktonic counterparts, whatever their growth phase (Dubois-Brissonnet et al., 2016). In addition, the spatialized environments in biofilms promote the generation and fixation of a phenotypic diversity compared to selection of only one or very few clones in well mixed environment (Traverse et al., 2013; Martin et al., 2016). The spatial distribution of the biofilm multiple phenotypes can be visualized within the biofilm thickness through the observation of different patterns of physiological characteristics (growth rate, mRNA, proteins synthesis or CsgD production) using for example Gfp reporter systems (Werner et al., 2004; Lenz et al., 2008; Stewart and Franklin, 2008; Serra et al., 2013).

Regulation of genes which differentiate planktonic and biofilm protein patterns are numerous and can be partitioned in several categories: metabolism (carbon catabolism, aerobic/anaerobic metabolism, membrane and transport), stress responses and adaptation, motility and attachment (flagellin, surface proteins), EPS production and quorum-sensing signaling (Whiteley et al., 2001; Sauer et al., 2002; Khemiri et al., 2016). Both transcriptional and post-transcriptional regulation occur: the first is slow but may be important for the long-term stability of the biofilm (Guttenplan and Kearns, 2013); the second is described to be mainly controlled by the c-di-GMP intracellular level. As mentioned previously, elevated intracellular levels of c-di-GMP generally promote EPS synthesis and biofilm formation, while decreased levels reduce biofilm formation (Martinez and Vadyvaloo, 2014).

Besides, biofilms can constitute an optimal environment for both cell to cell exchanges of genetic material and genetic mutations in biofilm inhabitants. They offer a panel of ideal characteristics for horizontal gene transfer through conjugation and transformation. These include the presence of high cell density favoring physical contact between biofilm bacteria and of a matrix that is rich in communication signals and in extracellular DNA (eDNA) (Madsen et al., 2012). In addition to providing transferable genetic elements (Hannan et al., 2010), the eDNA plays a central role in triggering natural competence in biofilm bacteria (Molin and Tolker-Nielsen, 2003). Horizontal gene transfer has therefore been described in several studies revealing that conjugation levels were 700–1000-fold higher in biofilms compared to planktonic bacterial cells (Król et al., 2013; Savage et al., 2013). This “permeability” of biofilm bacteria to heterologous mobile genetic elements is likely to shape the evolution of biofilm bacteria and to enhance their relatedness (Madsen et al., 2012). Another mechanism yielding genetic evolution in biofilms is linked to a higher mutation rate of certain biofilm bacteria. Important studies down this line have been performed in P. aeruginosa. Initial observations reported that genetic diversification occurred through a recA-dependant mechanism within short-term growth in biofilms and yielded mutants with multiple novel traits including motility, nutrition requirements, morphology, biofilm phenotypes, and stress resistance (Boles et al., 2004). The study of mutations in-situ within biofilms using a gfp gene containing a +1 frameshift mutation showed that mutations occurred in microcolony structures and increased at a frequency 100 to 1800-fold higher than that observed in planktonic cultures (Conibear et al., 2009). The underlying mechanism is linked to the mismatch repair system (MRS) which monitors the fidelity of DNA replication and recombination through its two main components MutS and MutL (Oliver et al., 2002). Using mutS deficient derivatives of P. aeruginosa and a flow-cell biofilm model system, Luján et al. (2011) showed that the mutants yielded enhanced phenotypic and morphological diversities over wild type strains in structured biofilms. Interestingly, the generated morphotypic variants showed increased competitiveness over the parental strain. This is to correlate to the high prevalence (30–60%) of mutator strains due to alterations in the mutS and mutL genes in P. aeruginosa chronic infections while detection of mutators is rare in P. aeruginosa acute infections (Gutiérrez et al., 2004; Feliziani et al., 2010).

Altogether, this overall genetic plasticity of bacteria in biofilm yields a rapid development of diversity among members of biofilm communities and is likely to shape the biofilm structure because of the co-development of the different morphologies and phenotypes. This provides the biofilm with what has been termed the “insurance hypothesis” in ecology that considers that the stability of many biological communities relies on their diversity which increases the chance that some members will be able to withstand environmental variations that the community may encounter (Boles et al., 2004). This enhanced clonal diversity in biofilms is a real challenge in the control of pathogen and detrimental biofilms as they may rapidly adapt to environmental stresses such as treatments with antimicrobials (Macià et al., 2011; Koch et al., 2014; Van Meervenne et al., 2014). In contrast, this diversity is a real benefit in biotechnological issues in which biofilms can be exploited in numerous applications and under many different environmental conditions (Berlanga and Guerrero, 2016; Piard and Briandet, 2016).

Multispecies biofilm is a result of cell–cell and cell–environment interactions such as cooperation, competition or exploitation that create heterogeneity in biofilms (Liu et al., 2016). These specific interactions between species are involved in the spatial organization of biofilms in which they are more favored than in planktonic environments. They maintain their diversity and stability by generating more physiological and functional heterogeneity (Nadell et al., 2009; Pamp et al., 2009; Rendueles and Ghigo, 2015; Kragh et al., 2016; Liu et al., 2016; Pande et al., 2016). Indeed, in specific environment, some species cannot form biofilm alone, but grow in association with others species in multispecies biofilm showing interspecific cooperation interactions between subpopulations (Palmer et al., 2001). Specific interactions and spatial organization within biofilm create fitness effect through social phenotypes. A telling example is the symbiotic two-species consortium formed by Pseudomonas putida and Acinetobacter sp. strain C6 which has evolved in a non-random spatial organization where P. putida exclusively attached and grew on pre-existent colonies formed by Acinetobacter sp. strain C6. Resulting evolved communities were characterized by an increased fitness and productivity (Hansen et al., 2007). Microscopic time-lapse observations revealed that cell clusters were arranged according to a uniform pattern and that such structure results from the moving along the surface and the fusion of early microcolonies (Haagensen et al., 2015). These observations illustrate the improvement of community fitness through the active spatial structuration of its individuals and theirs interactions, and thereby the stabilization of their symbiotic relations.

Similar observations were made by describing the evolution of communities derived from a clonal Burkholderia cenocepacia biofilms (Poltak and Cooper, 2011). The authors highlighted the emergence of three variants and their persistence in mixed communities displaying enhanced productivity than any monoculture. The authors demonstrated that such productivity gains were due to the asymmetrical cross-feeding between the different ecotypes and the expansion and restructuration of biofilm space that constructed new niches. Overall, the fitness of cooperative or competitive phenotypes largely depends on neighboring cells that finally influences the spatial arrangement of genotypes within biofilms (Nadell et al., 2016; Stubbendieck et al., 2016). Reciprocally, the spatial structuring of genotypes within biofilm greatly influences the evolution of social phenotypes (Nadell et al., 2016). Many social phenotypes are regulated by QS through the secretion of diffusible signaling peptide (Nadell et al., 2016; Perchat et al., 2016). Studies showed how interspecies QS may have a role in competition interactions. In a P. putida–P. aeruginosa mixed-species biofilm, it was demonstrated a spatial repulsion between the two isolates (Fernandez-Piñar et al., 2011; Bridier et al., 2014). Indeed, both populations secreted molecules which negatively alter the growth of each other; P. aeruginosa secreted quinolone, a QS signaling molecule which inhibits biofilm formation of P. putida, and in the same way, P. putida secreted putisolvin which is regulated by QS and inhibits P. aeruginosa biofilm formation (Diggle et al., 2003; Kuiper et al., 2004; Fernandez-Piñar et al., 2011; Bridier et al., 2014). Other systems can have an important role in interspecies interactions such as communication and transport including outer membrane vesicles (OMVs) (Wang et al., 2015). OMVs could promote bacterial interactions and thereby participate to the architectural integrity of biofilms (Schwechheimer and Kuehn, 2015). In Helicobacter pylori, Franciscella, P. aeruginosa, V. cholera and P. putida, vesicles are involved in biofilm formation by increasing hydrophobicity of cells surface and by participating to the matrix formation (Yonezawa et al., 2011; Baumgarten et al., 2012; van Hoek, 2013; Altindis et al., 2014; Murphy et al., 2014; Wang et al., 2015). OMVs can also have an interspecies interference property in biofilms when they are coupled with an antimicrobial action and alter bacteria in biofilms (Schooling and Beveridge, 2006). Species interactions contribute thus through various way to shape biofilm architecture. Actually, processes related to intra-species interactions, as for instance cell death, can also play a key role in biofilm structuring. Localized cell death is known to trigger wrinkle formation of biofilm by focusing mechanical forces and instigate vertical extending of the biofilm (Asally et al., 2012; Rendueles et al., 2014; Nadell et al., 2016). Overall, it has been showed that cell death plays an important role in the development of multicellular biofilms and the subsequent dispersal of surviving cells (Webb et al., 2003; Mai-Prochnow et al., 2004). In Bacillus subtilis biofilms, subpopulations of cells use a cannibalistic strategy involving the production and secretion of two toxins to lyse sensitive siblings which then provide nutrients for the cannibals. Interestingly, cannibal cells correspond to the subpopulation producing the extracellular matrix, the production of toxins and matrix being triggered by surfactin, a paracrine signal whose production is controlled by the QS signaling peptide ComX (Lopez et al., 2009). This process finally promotes matrix producer subpopulations and enables the development of biofilm structure through an increase of matrix production.

This extraordinary large diversity of means provides to microorganisms the ability to dynamically shape biofilm architecture and functions using complementary mechanisms. Numbers of processes involved in architecture plasticity are thus inter-related through complex regulation networks enabling the targeted adaptation through the sensing of a wide range of environmental conditions.

Within a biofilm, individual cells have the ability to monitor their direct environment (nutrients, pH, ionic strength, oxygen, surface…). The integration of these various external signals leads to specific cellular responses that can be exploited to alter the community structure/function.

In this line, Sauer et al. (2004) elegantly demonstrated that a sudden increase in carbon substrate or pH of the growing medium lead to significant change in P. aeruginosa biofilm structure. Changing the glutamate concentration of the media from 2 to 20 mM triggers a total loss of the biofilm tridimensional structure in less than 60 min. This massive loss of surface-associated biomass observed was correlated with the induction of a subpopulation of bacteria with an increased expression of flagella and a decreased expression of pilus, allowing their dispersal in the flow. Similarly, Staphylococcus epidermidis biofilm exposed to a high osmotic pressure (from 86 to 776 mM NaCl) decreased the average bacterial local number density by 10-fold (Stewart et al., 2013). Increasing the flow shear stress applied on P. aeruginosa biofilm reduced the formation of self-aggregating clusters, in particular through a significant down regulation of genes involved in extracellular polysaccharide synthesis (Crabbé et al., 2008; Dingemans et al., 2016). Exposing a gravity sewer biofilm to increasing shear stress (from 1.12 to 1.45 mPa) affected porosity of the biostructure (from 70 down to 55%) and reduced the chemical oxygen demand in the sewers from 40 to 32% (Xu et al., 2017). Growing the microaerophilic human pathogen Campylobacter jejuni under aerobic condition (20% O₂) stimulates the kinetic of biofilm development (Reuter et al., 2010) and the complexity in their architecture (Turonova et al., 2015). Desiccation of the biofilm occurs periodically in various environments including soils, industrial surfaces or hypersaline ponds (Habimana et al., 2014; Decho, 2016; Lennon and Lehmkuhl, 2016). In the latter environment, the EPS attains a glass state upon extreme desiccation that presumably protects the biofilm inhabitants and allows them to resume activities upon rehydratation. When grown at the air interface, Bacillus subtilis developed a biofilm protected by a hydrophobic raincoat layer formed by the BslA surface-active protein (Arnaouteli et al., 2016). This interfacial layer of water-repellent proteins also protects the biofilm inhabitants from ethanol and biocide action (Epstein et al., 2011). When the biofilm structure limits antimicrobial penetration and prevents the contact with the microbial target, exposition to pulsating waves of energy (e.g., ultrasonic waves) can amplify the antimicrobial effect. This so called bio-acoustic effect is likely associate with a deformation of the biofilm and a better penetration in the EPS of the toxic compounds (Qian et al., 1996; Peterson et al., 2015). Another often neglected environmental parameter to shape biofilm is the nature of the substratum. Greene et al. (2016) demonstrated that it was possible to alter the biofilm structure of Acinetobacter baumannii only by changing its carrier nature. While an important structured biofilm was able to grow in 4 days on polycarbonate coupons, only sparse adhering cells were visible in the same condition on glass (biofilm biovolume decreased from more than 2.5 to below 0.1 μm³/μm²). Not only the spatial arrangement of the cell were altered by the nature of the substratum, but also the bacterial physiology as reported by the live/dead ratio that ranged from less than 2 for biofilm grown on rubber to almost 8 for cell grown on stainless steel. Muszanska et al. (2012) demonstrated that coating silicone rubber with a brush polymer alters the biofilm structure (including a strong decrease in the polysaccharidic matrix) and the susceptibility to the gentamycin antibiotic. From those observations, authors suggested that the antimicrobial treatments of biofilm-associated infections could be more effective on material protected with such active antibiofilm coatings. Similarly, Valle et al. (2006) observed that treating abiotic surfaces with group II capsular polysaccharides drastically reduces both initial adhesion and biofilm architecture by important nosocomial pathogens.

All these examples illustrate the possibility to manipulate the structure/function association of microbial biofilms by controlling one (or a combination) of parameter(s) in their local environment.

External cues can be put in used to act both directly on the biofilm EPS properties or reprogram individual cell physiology and transcriptional expression patterns. A large palette of exogeneous enzymes has the ability to degrade specific moieties of the complex biofilm matrix. Those EPS-degrading enzymes can act specifically on extracellular polysaccharides (dispersin B), proteins (proteinase K, trypsin) or eDNA (DNase I) (Boles and Horswill, 2011). Cocktails of such enzymes are proposed in the food-industry to target persistent deleterious biofilms (Lequette et al., 2010; Nguyen and Burrows, 2014). Dispersin B that hydrolyzes the glycosidic linkages of PNAG was found to be efficient in a range of pathogenic bacteria and is being commercially developed as a wound care gel (Kaplan et al., 2003). Enzymes from bacteriophages can dissolve extracellular polysaccharides of the matrix and reverse the biofilm tolerance to antibiotics and other antimicrobial treatments (Chan and Abedon, 2015). Bacteriophage enzymes were able to reduce the alginate EPS viscosity by up to 40% in P. aeruginosa biofilm (Hanlon et al., 2001). Using purified EPS depolymerase isolated from an Enterobacter agglomerans bacteriophage, Skillman et al. (1998) demonstrated a change in the physical properties of the EPS from a two species biofilms resulting in the effective removal of both species. Another telling example is the use of the biosynthetic glycoside hydrolases PelAh and PslGh that were able to disrupt the spatial organization of a pre-existing P. aeruginosa biofilm within 1 h, potentiating the action of colistin and neutrophils (Baker et al., 2016). By targeting the cell wall, the hydrolases LySMP was able to reduce the biofilm structure of Streptococcus suis by more than 80% and facilitate the action of several antibiotics on sessile communities (Meng et al., 2011).

Amyloids fibers are the “neglected child” of the EPS matrix (Dueholm and Nielsen, 2016) while evidence is rinsing that those proteinous assemblages are important drivers of the matrix viscoelastic properties (Lembré et al., 2014). D-amino acids (with some controversy) and parthenolide were identified as molecular inhibitors targeting the polymerisation or anchorage to the cell wall of TasA, the main Bacillus subtilis EPS amyloid (Kolodkin-Gal et al., 2010; Leiman et al., 2013; Romero et al., 2013). P. aeruginosa produces cis-2-decenoic acid, a small messenger molecule responsible for the induction of the biofilm dispersion response in a range of Gram-negative and Gram-positive bacteria. It has been shown to alter biofilm structure and to reverse tolerance to conventional antimicrobial agents (Marques et al., 2015). The matrix reprogrammation can also be triggered by biofilm cells exposition to sublethal concentration of antimicrobials. Schilcher et al. (2016) observed that subinhibitory concentrations of clindamycin upregulated the expression of major biofilm-associated genes in S. aureus biofilm and shift the composition of the biofilm matrix toward higher eDNA content.

In addition to soluble molecular effectors, microorganisms are able to respond to organic and inorganic volatiles in their local headspace, some of which influencing their ability to form biofilm (Audrain et al., 2015). Nitric oxide (NO) is a volatile messenger able to trigger biofilm dispersion. Barraud et al. (2009) demonstrated that exposing a multispecies biofilms in water system to 500 nM sodium nitroprusside (NO donor) almost totally abolished the biofilm spatial organization, increasing by 20 the efficacy of the conventional chlorine treatment. On the opposite, ammonia, a volatile produced by many bacteria, stimulates biofilm formation in Bacillus licheniformis and other relatives (Nijland and Burgess, 2010). Similarly, it was showed that self-produced acetic acid was used as volatile signals to stimulate and coordinate the timing of biofilm formation in B. subtilis (Chen et al., 2015). This behavioral biofilm response triggered by odorant molecules was compared to olfaction; it opens doors to new biofilm control strategies based on airborne volatile metabolites.

As mentioned previously, biofilm architecture and functions are intimately related to their microbial content and the spatial repartition of their inhabitants. In, several fields including health, agriculture, food processing and environment, new strategies emerged to manipulate biofilm functions by guided biofilm ecology. The effectors of these approaches are selected organisms that can alter population structures in the targeted community such as bacteria, bacteriophages, molds, yeasts, microalgae, amoeba, and metazoans.

A family of microbial probiotics are put in used on the market to combat human biofilm-associated infections (Vuotto et al., 2014). Specific inhabitants of the oral microbiome such as Porphyromonas gingivalis are responsible of the production of unpleasant malodorant volatile sulfur compounds (halitosis) (Lee and Baek, 2014). Different reports described a beneficial long term effect of combining conventional oral mouthwashes chemical pretreatment with probiotic therapies involving lactic acid bacteria such as the bacteriocin producing Streptococcus salivarius K12 (Masdea et al., 2012; Jamali et al., 2016). Using an agent-based spatially explicit model approach, Bucci et al. (2011) demonstrated that the competitive dynamic of bacteriocin producing strain in a multispecies biofilm strongly depends on a single critical bacteriocin-range parameter that measures the threshold distance from a focal bacteriocin-producing cell whose fitness is higher than that of sensitive cell. Similarly, the biofilm of Aggregatibacter actinomycetemcomitans involved in chronic periodontal diseases was degraded after exposition to a Lactobacillus probiotic altering the biofilm structure (Jaffar et al., 2016). Lactobacillus rhamnosus GG and Lactococcus lactis HY449 both affect the spatial organization of model oral biofilms and reduced the count of oral pathogens in the community (Jiang et al., 2016; Kim and Lee, 2016). The most widespread use of probiotic is the treatment of gastrointestinal diseases. Rieu et al. (2014) demonstrated that a Lactobacillus-induced host immunomodulation response was strongly enhanced when the potential probiotic was cultivated as a structured biofilm in contrast with free-cells. This fundamental discovery leads to the exploration of new biofilm-based formulations to increase their in vivo beneficial effects (Cheow et al., 2014).

In the medical area, an emerging research field to overcome bacterial antibioresistance (super bugs) and chronic biofilm-associated infections (BAI) is the bacteriophage therapy (Maura and Debarbieux, 2011; Chan and Abedon, 2015). In the lab, bacteriophages were efficient in mice models to treat a (biofilm associated) P. aeruginosa acute lung infection (Debarbieux et al., 2010). Exposing Clostridium difficile colony biofilms to a cocktail of selected phages lead to the emergence of lysed zones and elongated cells morphotypes in the structure, but the loss of cell viability observed in early stages decreased with biofilm age (Nale et al., 2016). While highly effective on free-cells, the architecture of biofilm, the diversity of cell types and the presence of matrix likely limit the phages efficacy to treat chronic BAI. Only few human phase II trials explored this approach to treat human patient with only mitigated success (Wright et al., 2009). There is a clear need for larger scale trials and deeper research on phage and biofilm interactions in this promising emerging field (Servick, 2016).

From farms to forks, the microbiological control of raw and processed food through the food chain is still mainly ensure by the use of chemical products including pesticides, antibiotics or disinfectants. Their massive use raised some important environmental and health concerns and stressed out the need for alternative sustainable approaches. In the crop field, a recent paper pinpointed the biofilm mode of life as an important driver of the efficacy of microbial biocontrol agents (Pandin et al., 2017). Indeed, different studies showed evidence that biocontrol agent are able to form protective biofilms on crop that develop antagonistic properties against unwanted microorganisms (Zeriouh et al., 2014). The associated mechanisms likely involved many of the biofilm traits, including spatial competition, cell-cell signaling and the production of antimicrobials (Zhou et al., 2016). Spraying antagonistic Bacillus subtilis TSK1-1 or Bacillus amyloliquefaciens WG6-14 on citrus leaf surface alter the spatial organization and the density of Xanthomonas axonopodis pv. citri, a pathogenic bacteria involved in citrus canker (Huang et al., 2012). A comparative transcriptome analysis of the biocontrol agent Bacillus amyloliquefaciens FZB42 as response to biofilm formation showed an up regulation of the lci gene encoding an antimicrobial peptide, and of operons involved in the production of the extracellular matrix (Kröber et al., 2016). It was also shown that the architecture of those protective biofilm can be stimulated by plant metabolites such as root exudates (Espinosa-Urgel et al., 2002). Similar protecting biofilms are envisioned in the feed/food environments to protect livestock building and the surface of food processing equipments from pathogen persistence (Mariani et al., 2011; Piard and Briandet, 2016). Habimana et al. (2011) demonstrated using confocal imaging and a simplified individual based model that exposing sessile cells of Listeria monocytogenes to Lactococcus lactis engaged a spatial race to interfacial nutrients resulting in a total loss of the pathogen multiplication. It was also recently shown that motile bacilli can create transient pores in Staphylococcus aureus biofilms, sensitizing the pathogenic structure to biocide action (Houry et al., 2012).

The use of organisms to shape new biofilm functions is also emerging in environmental sciences. Derlon and his collaborators nicely demonstrated that predation mediated by added protozoa (Tetrahymena pyriformis) triggers strong architectural change of an ultrafiltration membrane biofilm (from flat to heterogeneous and porous structure), increasing by 2 the permeate flux (Derlon et al., 2012). The same group also demonstrated that metazoan worms, including the nematode Plectus aequalis and the oligochaetes Aelosoma hemprichi, were also able to remodel membrane fouling biofilm structure and to increase significantly the membrane efficacy (Derlon et al., 2013; Klein et al., 2016).

The microflora of stone monuments is mainly composed of microbial biofilms and lichens. Scientists of this field implicate these complex ecosystems in stone damage while others pinpointed their bioprotective role (Pinna, 2014). Application of biofilm-induced calcium carbonate precipitation is an emerging tool for the bioremineralisation of stone and cultural heritage (Dhami et al., 2014). Dick et al. (2006) evaluated the performance of Bacillus sphaericus biofilms to restore deteriorated Euville limestone, a stone used for building and sculpturing in France. They demonstrated an important surface colonization and the presence of dense calcium carbonate crystals on biofilms formed on the treated stone. Similar biocalcifying effect was observed with Bacillus subtilis on deteriorated globigerina limestone (Micallef et al., 2016).

Environmental biofilms are largely involved in global biogeochemical cycles (Singer et al., 2010). Through human intensive activities and the resulting environmental changes, we are unintentionally affecting and remodeling those natural ecosystems. At the Paris climate conference (COP21) in 2015, 195 countries adopted a legally binding global climate deal. The agreement sets out a global action plan to put the world on track to avoid dangerous climate change by limiting global warming to well below 2°C above pre-industrial levels (Rhodes, 2016). Indeed, a 2°C warming in flowing water is already enough to drive significant changes in freshwater biofilm structure/function by inducing a complex reorganization in the network of interactions among microbial populations within the biofilm matrix (Romani et al., 2014).