Biology subjects

Suarez, C.

Publications and source records attributed to Suarez, C..

15 recordsLinked to original sources

bioRxiv2026

Capping protein regulates the balance of assembly among diverse actin networks in C. elegans zygotes

Actin cytoskeleton networks exhibit specialized architectural properties for specific cellular tasks, as determined by the actin-binding proteins (ABPs) associated with each network. Proper allocation of a limiting pool of actin monomers also helps shape the assembly of different F-actin networks. The ABP capping protein (CP) modulates F-actin network architecture through regulation of actin filament length by capping filament barbed ends. Using a combination of in vitro biochemistry and quantitative live-cell imaging, we characterize CP as a major regulator of inter-network competition between filopodia and mini-comets, two F-actin networks in the one-cell C. elegans embryo (zygote). We establish that this regulation is facilitated in part by competition for binding barbed ends between CP and the F-actin elongator formin CYK-1. Together, these results reveal a role for CP in determining F-actin network architecture and dynamics, regulating the coordination between actin assembly factors to assemble and maintain different dynamic F-actin networks, and allocation of G-actin between competing cortical F-actin networks. Summary for table of contentsCells assemble diverse actin cytoskeleton networks within a common cytoplasm for essential cellular processes. Yde et al. establish a role for Capping Protein, a regulator of actin filament length, in coordinating the balanced assembly of distinct actin networks in the C. elegans zygote.

cell biology↗

bioRxiv2025

A revised model of nuclear actin import: Importin 9 competes with cofilin, profilin, and RanGTP for actin binding

While predominantly studied in cytoplasmic contexts, actin plays critical roles in the nucleus, regulating chromatin accessibility and remodeling, transcription, and DNA damage repair. Cell- based studies have contributed to a widely accepted model in which the import factor Importin 9 (IPO9) acts in concert with the actin filament-severing protein cofilin to transport actin into the nucleus. The classical nuclear localization signal on cofilin is thought to anchor IPO9 to cofilin- bound actin monomers, driving the formation of an import-competent tripartite actin*cofilin*IPO9 complex. In striking contradiction to this established model of actin import, we demonstrate that IPO9 directly binds to monomeric actin with mid-nanomolar affinity and, rather than promoting IPO9*actin complex formation, cofilin competitively inhibits binding of IPO9 to actin. We further report competitive binding for monomeric actin between IPO9 and the canonical actin monomer- sequestering protein, profilin. As cofilin and profilin are both capable of binding actin monomers at the barbed face, our results are consistent with a model in which IPO9 binds an overlapping portion of this interface. In further support, we demonstrate that IPO9 modestly occludes the barbed face of actin monomers, decreasing the rate of filament formation, and exhibits minimal filamentous actin binding. Finally, we identify unexpected affinity between the nuclear import release factor RanGTP and monomeric actin; however, a tripartite IPO9*actin*RanGTP complex does not form. The competitive interactions observed between IPO9 and cytoplasmic actin- binding proteins suggest dynamically coupled equilibria mediate the nuclear transport of actin monomers.

biochemistry↗

bioRxiv2025

Comparative analysis of the EF-1α Intergenic Region in Babesia divergens isolates: Insights into TA Repeat Variation and Potential Regulatory Implications

Babesia divergens, a zoonotic tick-borne pathogen, causes bovine and human babesiosis in Europe. The Elongation Factor 1 alpha (EF-1) protein is important in many cellular processes and has emerged as a possible target for subunit vaccine development against parasitic infections, and its intergenic region (IG) is an important tool for genetic manipulation of Babesia parasites. While the EF-1 locus of B. divergens has been described, structural variation between isolates was poorly defined. In order to fill this gap, we performed a comparative analysis of the EF-1-IG region in B. divergens human (Rouen 87, and Spanish sample), and bovine (Turkiye) host isolates. Our findings revealed both conserved and variable elements, particularly in TA nucleotide repeat numbers and IG sequence length. The Spanish isolate exhibited the highest TA repeat expansion, whereas the Rouen 87 strain had the shortest IG region. Given the known role of repeat-rich promoter elements in gene regulation, these differences may influence EF-1 transcription. Additionally, these findings provide insights into the evolutionary divergence of B. divergens and its host adaptation mechanisms. This study establishes a foundation for future gene editing and transfection strategies, where selecting intergenic sequences with varying TA repeats could optimize transfection efficiency and explain phenotypic differences between isolates from different hosts or regions.

genomics↗

bioRxiv2024

Evaluation of homologous recombination repair status in metastatic prostate cancer by next-generation sequencing and functional tissue-based immunofluorescence assays

PurposeMetastatic prostate cancer (mPC) is enriched for homologous recombination repair (HRR) gene alterations; these biomarkers have prognostic and predictive value. Next-generation sequencing (NGS) allows for patient stratification based on these biomarkers, but widespread clinical implementation is still limited. Moreover, not all mutations in HRR genes result in functional HRR loss in the tumor. We investigated the correlation between genomic and functional loss of HRR, using NGS and an optimized RAD51 immunofluorescence (RAD51-IF) assay in mPC clinical biopsies. Experimental designObservational study including patients with stage IV prostate cancer. Biopsies from either primary tumor or metastatic biopsies underwent NGS (targeted sequencing and/or whole-exome sequencing), and RAD51-IF. Clinical data was extracted from electronic patient records. Results219 biopsies from 187 patients were acquired, including primary (151/219) and metastatic (68/219) tumor biopsies collected either in the metastatic hormone- sensitive (169/219) or castration-resistant (50/219) setting. NGS (181 biopsies from 157 patients) showed frequent genomic alterations in TP53 (40%), AR (15%), PTEN (14%), MYC (10%), BRCA2 (9%), ATM (8%) and BRCA1 (2%). Tissue for RAD51 IF was available for 206 samples; of those, 140/206 (68%) were evaluable for RAD51- IF. Based on a previously defined threshold of 10% RAD51-positive cells, 21% samples had RAD51-low results compatible with HRR deficiency (HRD). Sample matched RAD51-IF and genomics data were obtained for 128 biopsies (117 patients): RAD51-IF had a high sensitivity (68%) and specificity (85%) to identify cases with BRCA1/2 alterations. Additionally, the RAD51-IF assay was able to identify restoration of HRR function in selected cases with BRCA2 reversion mutations or BRCA1 expression. ConclusionsRAD51-IF is feasible in routine clinical samples from mPC patients and associates strongly with clinically relevant HRR gene alterations.

cancer biology↗

bioRxiv2023

Multi-monoubiquitination controls VASP-mediated actin dynamics

The actin cytoskeleton performs multiple cellular functions, and as such, actin polymerization must be tightly regulated. We previously demonstrated that reversible, non-degradative ubiquitination regulates the function of the actin polymerase VASP in developing neurons. However, the underlying mechanism of how ubiquitination impacts VASP activity was unknown. Here we show that mimicking multi-monoubiquitination of VASP at K240 and K286 negatively regulates VASP interactions with actin. Using in vitro bio-chemical assays, we demonstrate the reduced ability of multi-monoubiquitinated VASP to bind, bundle, and elongate actin fil-aments. However, multi-monoubiquitinated VASP maintained the ability to bind and protect barbed ends from capping protein. Lastly, we demonstrate the introduction of recombinant multi-monoubiquitinated VASP protein altered cell spreading morphology. Collectively, these results suggest a mechanism in which ubiquitination controls VASP-mediated actin dynamics.

cell biology↗

bioRxiv2022

Ventral Hippocampal Infusions of C20:0 Ceramide Stimulate Microglia and Induce Anhedonia-like Behavior in Female and Male Rats

Increased long-chain C20:0 ceramides have been found in the serum of patients with depression. Moreover, ceramides are linked with increased microglia reactivity and inflammatory cytokine production, which are associated with depression. Since ceramides can readily cross the blood brain barrier, peripheral C20:0 ceramides could enter the brain, activate microglia, and induce depressive-like behavior. In this study, we determined whether localized infusion of C20:0 ceramides into the ventral hippocampus (VH) of rats is sufficient to activate microglia and induce depressive-like behaviors. Adult male and female rats received infusions of C20:0 ceramides or vehicle solution every other day for 2 weeks. After the third infusion, C20:0-infused animals showed reduced sucrose preference suggesting anhedonia-like behavior. However, 4-6 days after the last infusion, animals infused with C20:0 ceramides did not show anhedonia-like or despair-like behavior suggesting the behavioral effect was reversible. After the final behavioral test, C20:0-infused animals had more Iba-1+ microglia in the VH. Despite the increased number of VH microglia, the expression of inflammatory genes was not increased. In conclusion, our data suggest that localized increases in C20:0 ceramides in the VH are sufficient to induce microglia activation and reversible anhedonia-like behavior.

neuroscience↗

bioRxiv2022

The actin assembly requirements of the formin Fus1 to build the fusion focus

Formins form the largest family of actin filament nucleators and elongators, involved in the assembly of diverse actin structures. Actin filament nucleation and elongation activities reside in the formin homology 1 (FH1) and FH2 domains, common to all formins. However, the rate of these reactions varies between formins by at least 20-fold. Typically, each cell expresses several distinct formins, each contributing to the assembly of one or several actin structures, raising the question of what confers each formin its specificity. Here, using the formin Fus1 in the fission yeast Schizosaccharomyces pombe, we systematically probed the importance of formin nucleation and elongation rates for function in vivo. Fus1 assembles the actin fusion focus, an aster-like structure of actin filaments at the contact site between gametes, necessary for the process of cell fusion to form the zygote during sexual reproduction. By constructing chimeric formins with combinations of FH1 and FH2 domains previously characterized in vitro, we establish that changes in formin nucleation and elongation rates have direct consequences on the architecture of the fusion focus, and that Fus1 native high nucleation and low elongation rates are optimal for fusion focus assembly. We further describe a point mutant in the Fus1 FH2 domain that preserves native nucleation and elongation rates in vitro but alters function in vivo, indicating an additional property of the FH2 domain. Thus, rates of actin assembly are tailored for assembly of specific actin structures.

cell biology↗

bioRxiv2021

Disturbance-based management of ecosystem services and disservices in partial nitritation anammox biofilms

The resistance and resilience provided by functional redundancy, a common feature of microbial communities, is not always advantageous. An example is nitrite oxidation in partial nitritation-anammox (PNA) reactors during wastewater treatment, where suppression of nitrite oxidizers like Nitrospira is sought. In these ecosystems, biofilms provide microhabitats with oxygen gradients, allowing the coexistence aerobic and anaerobic bacteria. We designed a disturbance experiment where PNA biofilms treating water from a high rate activated sludge process removing organic matter (mainstream wastewater), were constantly or intermittently exposed to the effluent of anaerobic sewage sludge digestion dewatering (sidestream wastewater), which has been proposed to inhibit nitrite oxidizers. With increasing sidestream exposure we observed decreased abundance, alpha-diversity, functional versatility, and hence functional redundancy, among Nitrospira in the PNA biofilms, while the opposite patterns were observed for anammox bacteria within Brocadia. At the same time, species turnover was observed for the aerobic ammonia-oxidizing Nitrosomonas populations. The different exposure regimens were associated with metagenomic assembled genomes of Nitrosomonas, Nitrospira, and Brocadia, encoding genes related to N-cycling, substrate usage, and osmotic stress response, possibly explaining the three different patterns by niche differentiation. These findings imply that disturbances can be used to manage the functional redundancy of biofilm microbiomes in a desirable direction, which should be considered when designing operational strategies for wastewater treatment.

microbiology↗

bioRxiv2020

Profiling diverse sequence tandem repeats in colorectal cancer reveals co-occurrence of microsatellite and chromosomal instability involving Chromosome 8

Colorectal carcinomas (CRCs) which have lost DNA mismatch repair display hypermutability evident in a molecular phenotype called microsatellite instability (MSI). These mismatch repair deficient tumors are thought to lack widespread genomic instability features, such as copy number changes and rearrangements. To identify MSI for clinical diagnosis, current molecular testing looks for changes in mononucleotide or dinucleotide repeats. However, microsatellites have other types of sequence tandem repeats such as tri- and tetranucleotide motifs. These additional classes of microsatellites are generally not examined for MSI but are known to be unstable in a phenotype known as elevated microsatellite alterations at selected tetranucleotide repeats, or EMAST. We developed a sequencing approach that provides ultra-high coverage (>2500X) of microsatellite targets and cancer genes for profiling genomic instability. We assessed the diverse repeat motifs across 200 microsatellites. Our approach provides highly sensitive detection of MSI with high specificity, evaluates copy number alterations with high accuracy, delineates chromosomal instability (CIN) classification and deconvolutes subclonal architecture. By examining both MSI and CIN, we discovered mutations and copy number alterations that defined mixed genomic instability states of CIN and MSI, which are normally considered exclusive. An increase in copy number of chromosome arm 8q was prevalent among MSI tumors. Moreover, we identified an inter-chromosomal translocation event from a CRC with co-occurrence of MSI. Subclonal analysis demonstrated that mutations which are typically considered to be exclusive in MSI, shows mutual occurrence in MSI tumors with more sensitive characterization. Our approach revealed that MSH3 mutations are a potential source of mixed genomic instability features. Overall, our study demonstrates that some colorectal cancers have features of both microsatellite and chromosomal instability. This result may have implications for immunotherapy treatment.

genomics↗

bioRxiv2020

The cellular genomic diversity, regulatory states and networking of the metastatic colorectal cancer microenvironment

PurposeThe liver is the most frequent metastatic site for colorectal cancer (CRC). Its microenvironment is modified to provide a niche that allows CRC cell growth. This study focused on characterizing the cellular changes in the metastatic CRC (mCRC) liver tumor microenvironment (TME). Experimental DesignWe analyzed a series of microsatellite stable (MSS) mCRCs to the liver, paired normal liver tissue and peripheral blood mononuclear cells using single cell RNA-seq (scRNA-seq). We validated our findings using multiplexed spatial imaging and bulk gene expression with cell deconvolution. ResultsWe identified TME-specific SPP1-expressing macrophages with altered metabolism features, foam cell characteristics and increased activity for extracellular matrix (ECM) organization. SPP1+ macrophages and fibroblasts expressed complementary ligand receptor pairs with the potential to mutually influence their gene expression programs. TME lacked dysfunctional CD8 T cells and contained regulatory T cells, indicative of immunosuppression. Spatial imaging validated these cell states in the TME. Moreover, TME macrophages and fibroblasts had close spatial proximity, a requirement for intercellular communication and networking. In an independent cohort of mCRCs in the liver, we confirmed the presence of SPP1+ macrophages and fibroblasts using gene expression data. An increased proportion of TME fibroblasts was associated with worst prognosis in these patients. ConclusionsWe demonstrated that mCRC in the liver is characterized by transcriptional alterations of macrophages in the TME. Intercellular networking between macrophages and fibroblasts supports CRC growth in the immunosuppressed metastatic niche in the liver. These features can be used to target these immune checkpoint resistant MSS tumors. TRANSLATIONAL RELEVANCEThe liver is the commonest site for metastatic colorectal cancer (mCRC). Alterations in the tumor microenvironment (TME) allow metastatic cells to seed the distant liver site and grow. Leveraging single-cell RNA sequencing, we discovered a distinct SPP1+ macrophage cell state with pro-fibrogenic gene expression and altered metabolism. These SPP1+ macrophages communicated with fibroblasts, mutually influencing each others gene expression program. Using spatial imaging, we confirmed proximal colocalization between macrophages and fibroblasts in the mCRC TME, which is required for intercellular communication. These states and intercellular communication promoted immunosuppression in the TME, with a lack of dysfunctional anti-tumor CD8 T cells and prevalence of regulatory T cells. Increased fibroblasts were associated with worst prognosis in an independent patient cohort. Our results identified novel TME features that result in reshaping of the metastatic niche that allows progression of mCRC. These features can be potential targets for mCRC treatment, which is microsatellite stable and resistant to immune checkpoint blockade.

cancer biology↗

bioRxiv2020

Diversity and gene expression patterns of functional groups in sidestream and mainstream wastewater partial-nitritation anammox biofilms

Partial nitritation-anammox (PNA) is today used for nitrogen removal from highly concentrated wastewater after anaerobic sludge digestion (sidestream). However, implementation of PNA for treatment of municipal wastewater (mainstream), with its lower ammonium concentration and lower temperature is challenging, which might be due to differences in microbial community composition and/or activity. To investigate this, we compared side-by-side sidestream and mainstream PNA biofilms using amplicon sequencing of 16S rDNA and rRNA, hzsB DNA and mRNA, and the genes nxrB, and amoA. The two communities were different to each other with relatively more heterotrophic denitrifying bacteria and less anammox bacteria in the mainstream. With hzsB and nxrB we found microdiversity among Brocadia and Nitrospira, and turnover (taxa replacement) between sidestream and mainstream. However, in both environments Brocadia sapporoensis represented most of the hzsB DNA and mRNA reads, despite the different environmental conditions and nitrogen removal rates. All of those populations present in both sidestream and mainstream had no differences in their 16S rRNA:rDNA ratios, supporting recent findings that rRNA:rDNA ratios are poor indicators of bacterial activity. The observed diversity within functional groups and composition differences between sidestream and mainstream add complexity to our view of PNA communities with possible implication for reactor function.

microbiology↗

bioRxiv2020

Evolutionary diverse LIM domain-containing proteins bind stressed actin filaments through a conserved mechanism

The actin cytoskeleton assembles into diverse load-bearing networks including stress fibers, muscle sarcomeres, and the cytokinetic ring to both generate and sense mechanical forces. The LIM (Lin11, Isl-1 & Mec-3) domain family is functionally diverse, but most members can associate with the actin cytoskeleton with apparent force-sensitivity. Zyxin rapidly localizes via its LIM domains to failing stress fibers in cells, known as strain sites, to initiate stress fiber repair and maintain mechanical homeostasis. The mechanism by which these LIM domains associate with stress fiber strain sites is not known. Additionally, it is unknown how widespread strain sensing is within the LIM protein family. We observe that many, but not all, LIM domains from functionally diverse proteins localize to spontaneous or induced stress fiber strain sites in mammalian cells. Additionally, the LIM domain region from the fission yeast protein paxillin like 1 (Pxl1) also localizes to stress fiber strain sites in mammalian cells, suggesting that the strain sensing mechanism is ancient and highly conserved. Sequence analysis and mutagenesis of the LIM domain region of zyxin indicate a requirement of tandem LIM domains, which contribute additively, for sensing stress fiber strain sites. In vitro, purified LIM domains from mammalian zyxin and fission yeast Pxl1 bind to mechanically stressed F-actin networks but do not associate with relaxed actin filaments. We propose that tandem LIM domains recognize an F-actin conformation that is rare in the relaxed state but is enriched in the presence of mechanical stress.

cell biology↗

bioRxiv2019

Single cell genomic characterization reveals the cellular reprogramming of the gastric tumor microenvironment

PurposeThe tumor microenvironment (TME) consists of a heterogenous cellular milieu that can influence cancer cell behavior. The characteristics of the cellular TME have a dramatic impact on treatments such as immunotherapy. These features can be revealed with single-cell RNA sequencing (scRNA-seq). We hypothesized that single cell gene expression studies of gastric cancer (GC) together with paired normal tissue and peripheral blood mononuclear cells (PBMCs) would identify critical elements of cellular dysregulation not apparent with other approaches.\n\nMethodsSingle cell gene expression studies were conducted on seven patients with GC and one patient with intestinal metaplasia. We sequenced 56,167 cells comprising GC (32,407 cells), paired normal tissue (18,657 cells) and PBMCs (5,103 cells). Protein expression of genes of interest was validated by multiplex immunofluorescence.\n\nResultsTumor epithelium had copy number alterations and a distinct gene expression program compared to normal with intra-tumor heterogeneity. The GC TME was significantly enriched for stromal cells, macrophages, dendritic cells (DCs) and Tregs. TME-exclusive stromal cells expressed extracellular matrix components distinct from normal tissue. Macrophages were transcriptionally heterogenous and did not conform to a binary M1/M2 paradigm. Gene expression program of tumor DCs was unique from PBMC DCs. TME-specific cytotoxic T cells comprised of two exhausted heterogenous subsets. Helper, cytotoxic T, Treg and NK cells expressed multiple immune checkpoint or costimulatory molecules. Receptor-ligand analysis revealed TME-exclusive inter-cellular communication.\n\nConclusionsSingle cell gene expression studies revealed widespread reprogramming across multiple cellular elements in the milieu of the GC TME. Cellular remodeling was delineated by changes in cell numbers, transcriptional states and inter-cellular interactions. This characterization facilitates understanding of tumor biology and enables the identification of novel molecular targets including for cancer immunotherapy.\n\nSTATEMENT OF TRANSLATIONAL RELEVANCEWe leveraged the power of single-cell genomics to characterize the heterogenous cell types and states in the tumor microenvironment (TME). By profiling thousands of single cells from surgical resections of gastric cancer together with paired normal mucosa and peripheral blood mononuclear cells (PBMCs), we determined the deviations in the TME from physiological conditions. Our analysis revealed a cellular reprogramming of the TME compared to normal mucosa in immune and stromal lineages. We detected transcriptional heterogeneity within macrophages and a TME-specific gene expression program in dendritic cells. Cytotoxic T cells in the TME had heterogenous profiles of exhaustion and expression of multiple immune checkpoint and costimulatory molecules. We constructed a receptor-ligand based inter-cellular communications network that was exclusive to tumor tissue. These discoveries provide information at a highly granular cellular resolution enabling advances in cancer biology, biomarker discovery and identification of treatment targets such as for immunotherapy.

cancer biology↗

bioRxiv2018

Mechanical and kinetic factors drive sorting of F-actin crosslinkers on bundles

In cells, actin binding proteins (ABPs) sort to different regions in order to establish F-actin networks with diverse functions, including filopodia used for cell migration, or contractile rings required for cell division. Recent experimental work uncovered a passive mechanism that may facilitate spatial localization of ABPs: binding of a short crosslinker protein to two actin filaments promotes the binding of other short crosslinkers and inhibits the binding of longer crosslinkers (and vice versa). We hypothesize this sorting arises because F-actin is semiflexible and cannot bend over short distances. We develop a mathematical theory and a kinetic Monte Carlo simulation encompassing the most important physical parameters for this process, and use simulations of a coarse-grained but molecularly explicit model to characterize and test our predictions about the interplay of mechanical and kinetic parameters. Our theory and data predict an explicit dependence of crosslinker separation on bundle polymerization rate. We perform experiments that confirm a dependence on polymerization rate, but in an unanticipated non-monotonic manner. We use simulations to show that this non-monotonic behavior can arise in situations where crosslinkers have equal bundling affinity at equilibrium, but differing microscopic binding rates to filaments. This dependence of sorting on actin polymerization rate is a non-equilibrium effect, qualitatively similar to non-equilibrium domain formation in materials growth. Thus our results reveal an avenue by which cells can organize molecular material to drive biological processes, and can also guide the choice and design of crosslinkers for engineered protein-based materials.

biophysics↗

bioRxiv2018

Biofilm thickness matters: Deterministic assembly of different functions and communities in nitrifying biofilms

Microbial biofilms are important in natural ecosystems and in biotechnological applications. Biofilm architecture influences organisms spatial positions, who their neighbors are, and redox gradients, which in turn determine functions. We ask if and how biofilm thickness influences community composition, architecture and functions. But biofilm thickness cannot easily be isolated from external environmental factors. We designed a metacommunity system in a wastewater treatment plant, where either 50 or 400 {micro}m thick nitrifying biofilms were grown simultaneously on biofilm carriers in the same reactor. Model simulations showed that the 50 {micro}m biofilms could be fully oxygenated whereas the 400 {micro}m biofilms contained anaerobic zones. The 50 and 400 {micro}m biofilms developed significantly different communities. due to deterministic factors were stronger than homogenizing dispersal forces in the reactor, despite the fact that biofilms experienced the same history and external conditions. Relative abundance of aerobic nitrifiers was higher in the 50 {micro}m biofilms, while anaerobic ammonium oxidizers were more abundant in the 400 {micro}m biofilms. However, turnover was larger than the nestedness component of between-group beta-diversity, i.e. the 50 {micro}m biofilm was not just a subset of the thicker 400 {micro}m biofilm with reduced taxa richness. Furthermore, the communities had different nitrogen transformation rates. The study shows that biofilm thickness has a strong impact on community composition and ecosystem function, which has implications for biotechnological applications, and for our general understanding of biofilms.\n\nIMPORTANCEMicroorganisms colonize all surfaces in water and form biofilms. Diffusion limitations form steep gradients of energy and nutrient sources from the water phase into the deeper biofilm parts, influencing community composition through the biofilm. Thickness of the biofilm will affect diffusion gradients, and is therefore presumably important for biofilm composition. Since environmental factors determine thickness, studies of how thickness influences biofilm functions and community assembly, have been difficult to perform. We studied biofilms for wastewater treatment with fixed thicknesses of 50 and 400 {micro}m during otherwise similar conditions and history. Despite growing in the same wastewater reactor, 16S rRNA gene sequencing and confocal microscopy showed the formation of two different communities, performing different ecosystem functions. Using statistical methods, we show for the first time, how biofilm thickness influences community assembly. The results help our understanding of the ecology of microbial biofilms, and in designing engineered systems based on ecological principles.

microbiology↗