scholarly journals Multidrug Resistance Regulators MarA, SoxS, Rob, and RamA Repress Flagellar Gene Expression and Motility in Salmonella enterica Serovar Typhimurium

2019 ◽  
Vol 201 (23) ◽  
Author(s):  
Srinivas S. Thota ◽  
Lon M. Chubiz
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Multidrug Resistance ◽  
Related Species ◽  
Salmonella Enterica ◽  
Mrna Translation ◽  
Flagellar Gene ◽  
Content Type ◽  
E Coli ◽  
Serovar Typhimurium

ABSTRACT Production of flagella is costly and subject to global multilayered regulation, which is reflected in the hierarchical control of flagellar production in many bacterial species. For Salmonella enterica serovar Typhimurium and its relatives, global regulation of flagellar production primarily occurs through the control of flhDC transcription and mRNA translation. In this study, the roles of the homologous multidrug resistance regulators MarA, SoxS, Rob, and RamA (constituting the mar-sox-rob regulon in S. Typhimurium) in regulating flagellar gene expression were explored. Each of these regulators was found to inhibit flagellar gene expression, production of flagella, and motility. To different degrees, repression via these transcription factors occurred through direct interactions with the flhDC promoter, particularly for MarA and Rob. Additionally, SoxS repressed flagellar gene expression via a posttranscriptional pathway, reducing flhDC translation. The roles of these transcription factors in reducing motility in the presence of salicylic acid were also elucidated, adding a genetic regulatory element to the response of S. Typhimurium to this well-characterized chemorepellent. Integration of flagellar gene expression into the mar-sox-rob regulon in S. Typhimurium contrasts with findings for closely related species such as Escherichia coli, providing an example of plasticity in the mar-sox-rob regulon throughout the Enterobacteriaceae family. IMPORTANCE The mar-sox-rob regulon is a large and highly conserved stress response network in the Enterobacteriaceae family. Although it is well characterized in E. coli, the extent of this regulon in related species is unclear. Here, the control of costly flagellar gene expression is connected to the mar-sox-rob regulon of S. Typhimurium, contrasting with the E. coli regulon model. These findings demonstrate the flexibility of the mar-sox-rob regulon to accommodate novel regulatory targets, and they provide evidence for its broader regulatory role within this family of diverse bacteria.

scholarly journals SoxS represses flagellar gene expression through RflP in Salmonella enterica Serovar Typhimurium

2020 ◽  
Author(s):  
Srinivas S. Thota ◽  
Brittany N. Henry ◽  
Lon M. Chubiz
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Transcription Factors ◽  
Salmonella Enterica ◽  
Response Regulator ◽  
Flagellar Gene ◽  
Treatment And Prevention ◽  
Intracellular Signals ◽  
Serovar Typhimurium ◽  
Close Relatives

ABSTRACTFlagellar gene expression is subject to regulation by many global transcription factors in response to environmental and nutritional signals. One of the primary ways this occurs in Salmonella enterica serovar Typhimurium, and its close relatives, is through controlling levels of FlhD4C2 (the flagellar master regulator) via transcriptional, post-transcriptional, and post-translational mechanisms. Recently, we found the homologous transcription factors MarA, Rob, and SoxS repress flhDC expression by distinct mechanisms. MarA and Rob, regulators involved in inducible multidrug resistance, repressed flhDC transcription by interacting directly with the flhDC promoter. Alternatively, SoxS, the oxidative stress response regulator, altered FlhD4C2 levels independent of flhDC transcription by post-transcriptional or post-translational mechanism. Here, using a forward genetic screen, we discovered that SoxS-dependent repression of flagellar gene expression occurs through RflP, an anti-FlhD4C2 factor that targets FlhD4C2 for proteolytic degradation. Elevated soxS expression resulted in concomitant increases in rflP expression, indicating SoxS may work through RflP at the level of rflP transcription. Mapping of the rflP promoter and a bioinformatic search yielded a putative SoxS binding site proximal to the rflP transcription start site. Comparison of the rflP promoter region in S. Typhimurium and Escherichia coli indicate substantial differences, providing a possible mechanism for differential expression of rflP between these species.IMPORTANCESalmonella enterica is a major cause of foodborne illness. Understanding environmental and intracellular signals used by Salmonella to control expression of virulence-associated traits is critical to advancing treatment and prevention of Salmonella-related disease. Reduced expression of flagella at key points during Salmonella infection aids in evasion of the host innate immune system. Within macrophages Salmonella is non-flagellated and exposed to oxidative stress. SoxS-dependent repression of flagellar genes may provide a potential link between oxidative stress and reductions in flagellar expression.

scholarly journals Facultative Anaerobes Shape Multispecies Biofilms Composed of Meat Processing Surface Bacteria and Escherichia coli O157:H7 or Salmonella enterica Serovar Typhimurium

2019 ◽  
Vol 85 (17) ◽  
Author(s):  
Jeyachchandran Visvalingam ◽  
Hui Wang ◽  
Tim C. Ells ◽  
Xianqin Yang
Keyword(s):  
Food Processing ◽  
Salmonella Enterica ◽  
Biofilm Formation ◽  
Single Species ◽  
Meat Processing ◽  
Content Type ◽  
E Coli ◽  
Facultative Anaerobes ◽  
Serovar Typhimurium ◽  
Multispecies Biofilms

ABSTRACT This study investigated the microbial dynamics in multispecies biofilms of Escherichia coli O157:H7 strain 1934 (O157) or Salmonella enterica serovar Typhimurium ATCC 14028 (ST) and 40 strains of meat processing surface bacteria (MPB). Biofilms of O157 or ST with/without MPB were developed on stainless steel coupons at 15°C for up to 6 days. Bacteria in suspensions (inoculum, days 2 and 6) and biofilms (days 2 and 6) were enumerated by plating. The composition of multispecies cultures was determined by 16S rRNA gene sequencing. In suspensions, levels of O157 and ST were ∼2 log higher in single-species than in multispecies cultures on both sampling days. ST was 3 log higher in single-species than in multispecies biofilms. A similar trend, though to a lesser extent, was observed for O157 in biofilms on day 2 but not on day 6. No difference (P > 0.05) in bacterial counts was noted for the two MPB-pathogen cocultures at any time during incubation. Bacterial diversity in multispecies cultures decreased with incubation time, irrespective of the pathogen or culture type. The changes in the relative abundance of MPB were similar for the two MPB-pathogen cocultures, though different interbacterial interactions were noted. Respective fractions of ST and O157 were 2.1% and 0.97% initially and then 0.10% and 0.07% on day 2, and 0.60% and 0.04% on day 6. The relative proportions of facultative anaerobes in both multispecies cultures were greater in both suspensions and biofilms than in the inoculum. Citrobacter, Hafnia, Aeromonas, and Carnobacterium predominated in biofilms but not always in the planktonic cultures. IMPORTANCE Results of this study demonstrate that Salmonella enterica serovar Typhimurium and E. coli O157:H7 can integrate into biofilms when cocultured with bacteria from meat plant processing surfaces. However, the degree of biofilm formation for both pathogens was substantially reduced in the presence of the competing microbiota, with S. Typhimurium more greatly affected than E. coli O157:H7. The expression of extracellular determinants such as curli and cellulose appears to be less important for biofilm formation of the pathogens in multispecies cultures than in monoculture. In contrast to previous reports regarding food processing surface bacteria, data collected here also demonstrate that facultative anaerobes may have a competitive edge over strict aerobes in establishing multispecies biofilms. It would be important to take into account the presence of background bacteria when evaluating the potential persistence of a pathogen in food processing facilities.

scholarly journals Salmonella enterica Serovar Typhimurium SPI-1 and SPI-2 Shape the Global Transcriptional Landscape in a Human Intestinal Organoid Model System

mBio ◽  
2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Anna-Lisa E. Lawrence ◽  
Basel H. Abuaita ◽  
Ryan P. Berger ◽  
David R. Hill ◽  
Sha Huang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Intestinal Epithelium ◽  
Salmonella Enterica ◽  
Secretion System ◽  
Host Responses ◽  
Secretion Systems ◽  
Content Type ◽  
Serovar Typhimurium ◽  
Type 3

ABSTRACT The intestinal epithelium is a primary interface for engagement of the host response by foodborne pathogens, like Salmonella enterica Typhimurium. While the interaction of S. Typhimurium with the mammalian host has been well studied in transformed epithelial cell lines or in the complex intestinal environment in vivo, few tractable models recapitulate key features of the intestine. Human intestinal organoids (HIOs) contain a polarized epithelium with functionally differentiated cell subtypes, including enterocytes and goblet cells and a supporting mesenchymal cell layer. HIOs contain luminal space that supports bacterial replication, are more amenable to experimental manipulation than animals and are more reflective of physiological host responses. Here, we use the HIO model to define host transcriptional responses to S. Typhimurium infection, also determining host pathways dependent on Salmonella pathogenicity island-1 (SPI-1)- and -2 (SPI-2)-encoded type 3 secretion systems (T3SS). Consistent with prior findings, we find that S. Typhimurium strongly stimulates proinflammatory gene expression. Infection-induced cytokine gene expression was rapid, transient, and largely independent of SPI-1 T3SS-mediated invasion, likely due to continued luminal stimulation. Notably, S. Typhimurium infection led to significant downregulation of host genes associated with cell cycle and DNA repair, leading to a reduction in cellular proliferation, dependent on SPI-1 and SPI-2 T3SS. The transcriptional profile of cell cycle-associated target genes implicates multiple miRNAs as mediators of S. Typhimurium-dependent cell cycle suppression. These findings from Salmonella-infected HIOs delineate common and distinct contributions of SPI-1 and SPI-2 T3SSs in inducing early host responses during enteric infection and reinforce host cell proliferation as a process targeted by Salmonella. IMPORTANCE Salmonella enterica serovar Typhimurium (S. Typhimurium) causes a significant health burden worldwide, yet host responses to initial stages of intestinal infection remain poorly understood. Due to differences in infection outcome between mice and humans, physiological human host responses driven by major virulence determinants of Salmonella have been more challenging to evaluate. Here, we use the three-dimensional human intestinal organoid model to define early responses to infection with wild-type S. Typhimurium and mutants defective in the SPI-1 or SPI-2 type-3 secretion systems. While both secretion system mutants show defects in mouse models of oral Salmonella infection, the specific contributions of each secretion system are less well understood. We show that S. Typhimurium upregulates proinflammatory pathways independently of either secretion system, while the downregulation of the host cell cycle pathways relies on both SPI-1 and SPI-2. These findings lay the groundwork for future studies investigating how SPI-1- and SPI-2-driven host responses affect infection outcome and show the potential of this model to study host-pathogen interactions with other serovars to understand how initial interactions with the intestinal epithelium may affect pathogenesis.

scholarly journals Corrected Genome Annotations Reveal Gene Loss and Antibiotic Resistance as Drivers in the Fitness Evolution of Salmonella enterica Serovar Typhimurium

2016 ◽  
Vol 198 (23) ◽  
pp. 3152-3161 ◽  
Author(s):  
Sandip Paul ◽  
Evgeni V. Sokurenko ◽  
Sujay Chattopadhyay
Keyword(s):  
Multidrug Resistance ◽  
Salmonella Enterica ◽  
Gene Loss ◽  
Bacterial Genome ◽  
Genomic Islands ◽  
Genomic Diversity ◽  
Content Type ◽  
Chromosomal Genes ◽  
Serovar Typhimurium ◽  
Genome Annotations

ABSTRACT Horizontal acquisition of novel chromosomal genes is considered to be a key process in the evolution of bacterial pathogens. However, the identification of gene presence or absence could be hindered by the inconsistencies in bacterial genome annotations. Here, we performed a cross-annotation of omnipresent core and mosaic accessory genes in the chromosome of Salmonella enterica serovar Typhimurium across a total of 20 fully assembled genomes deposited into GenBank. Cross-annotation resulted in a 32% increase in the number of core genes and a 3-fold decrease in the number of genes identified as mosaic genes (i.e., genes present in some strains only) by the original annotation. Of the remaining noncore genes, the vast majority were prophage genes, and 255 of the nonphage genes were actually of core origin but lost in some strains upon the emergence of the S . Typhimurium serovar, suggesting that the chromosomal portion of the S . Typhimurium genome acquired a very limited number of novel genes other than prophages. Only horizontally acquired nonphage genes related to bacterial fitness or virulence were found in four recently sequenced isolates, all located on three different genomic islands that harbor multidrug resistance determinants. Thus, the extensive use of antimicrobials could be the main selection force behind the new fitness gene acquisition and the emergence of novel Salmonella pathotypes. IMPORTANCE Significant discrepancies in the annotations of bacterial genomes could mislead the conclusions about evolutionary origin of chromosomal genes, as we demonstrate here via a cross-annotation-based analysis of Salmonella Typhimurium genomes from GenBank. We conclude that despite being able to infect a broad range of vertebrate hosts, the genomic diversity of S . Typhimurium strains is almost exclusively limited to gene loss and the transfer of prophage DNA. Only nonphage chromosomal genes acquired after the emergence of the serovar are linked to the genomic islands harboring multidrug resistance factors. Since the fitness factors could lead to increased virulence, this poses an important research question: could overuse or misuse of antimicrobials act as selection forces for the emergence of more pathogenic strains of Salmonella ?

scholarly journals The Acyl Homoserine Lactone Receptor, SdiA, of Escherichia coli and Salmonella enterica Serovar Typhimurium Does Not Respond to Indole

2012 ◽  
Vol 78 (15) ◽  
pp. 5424-5431 ◽  
Author(s):  
Anice Sabag-Daigle ◽  
Jitesh A. Soares ◽  
Jenée N. Smith ◽  
Mohamed E. Elmasry ◽  
Brian M. M. Ahmer
Keyword(s):  
Escherichia Coli ◽  
Salmonella Enterica ◽  
Biofilm Formation ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Homoserine Lactone ◽  
Acyl Homoserine Lactone ◽  
Content Type ◽  
E Coli ◽  
Serovar Typhimurium ◽  
High Concentrations

ABSTRACTIn this study, we tested the hypothesis that the SdiA proteins ofEscherichia coliandSalmonella entericaserovar Typhimurium respond to indole. While indole was found to have effects on gene expression and biofilm formation, these effects were notsdiAdependent. However, high concentrations of indole did inhibitN-acyl-l-homoserine lactone (AHL) sensing by SdiA. We conclude that SdiA does not respond to indole but indole can inhibit SdiA activity inE. coliandSalmonella.

scholarly journals FimA, FimF, and FimH Are Necessary for Assembly of Type 1 Fimbriae on Salmonella enterica Serovar Typhimurium

2012 ◽  
Vol 80 (9) ◽  
pp. 3289-3296 ◽  
Author(s):  
Sarah A. Zeiner ◽  
Brett E. Dwyer ◽  
Steven Clegg
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Food Poisoning ◽  
Enteric Bacteria ◽  
Transcriptional Unit ◽  
Content Type ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Serovar Typhimurium

ABSTRACTSalmonella entericaserovar Typhimurium is a Gram-negative member of the familyEnterobacteriaceaeand is a common cause of bacterial food poisoning in humans. The fimbrial appendages are found on the surface of many enteric bacteria and enable the bacteria to bind to eukaryotic cells.S. Typhimurium type 1 fimbriae are characterized by mannose-sensitive hemagglutination and are assembled via the chaperone/usher pathway.S. Typhimurium type 1 fimbrial proteins are encoded by thefimgene cluster (fimAICDHFZYW), withfimAICDHFexpressed as a single transcriptional unit. The structural components of the fimbriae are FimA (major subunit), FimI, FimH (adhesin), and FimF (adaptor). In order to determine which components are required for fimbrial formation inS. Typhimurium, mutations infimA,fimI,fimH, andfimFwere constructed and examined for their ability to produce surface-assembled fimbriae.S. Typhimurium SL1344ΔfimA, -ΔfimH, and -ΔfimFmutants were unable to assemble fimbriae, indicating that these genes are necessary for fimbrial production inS. Typhimurium. However, SL1344ΔfimIwas able to assemble fimbriae. InEscherichia colitype 1 and Pap fimbriae, at least two adaptors are expressed in addition to the adhesins. However,E. colitype 1 and Pap fimbriae have been reported to be able to assemble fimbriae in the absence of these proteins. These results suggest differences between theS. Typhimurium type 1 fimbrial system and theE. colitype 1 and Pap fimbrial systems.

scholarly journals Binding of the RamR Repressor to Wild-Type and Mutated Promoters of theramAGene Involved in Efflux-Mediated Multidrug Resistance in Salmonella enterica Serovar Typhimurium

2011 ◽  
Vol 56 (2) ◽  
pp. 942-948 ◽  
Author(s):  
Sylvie Baucheron ◽  
Franck Coste ◽  
Sylvie Canepa ◽  
Marie-Christine Maurel ◽  
Etienne Giraud ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Dna Binding ◽  
Binding Site ◽  
Salmonella Enterica ◽  
Transcriptional Start Site ◽  
Local Level ◽  
Wild Type ◽  
Binding Model ◽  
Content Type ◽  
Serovar Typhimurium

ABSTRACTThe transcriptional activator RamA is involved in multidrug resistance (MDR) by increasing expression of the AcrAB-TolC RND-type efflux system in several pathogenicEnterobacteriaceae. InSalmonella entericaserovar Typhimurium (S.Typhimurium),ramAexpression is negatively regulated at the local level by RamR, a transcriptional repressor of the TetR family. We here studied the DNA-binding activity of the RamR repressor with theramApromoter (PramA). As determined by high-resolution footprinting, the 28-bp-long RamR binding site covers essential features of PramA, including the −10 conserved region, the transcriptional start site oframA, and two 7-bp inverted repeats. Based on the RamR footprint and on electrophoretic mobility shift assays (EMSAs), we propose that RamR interacts with PramAas a dimer of dimers, in a fashion that is structurally similar to the QacR-DNA binding model. Surface plasmon resonance (SPR) measurements indicated that RamR has a 3-fold-lower affinity (KD[equilibrium dissociation constant] = 191 nM) for the 2-bp-deleted PramAof an MDRS.Typhimurium clinical isolate than for the wild-type PramA(KD= 66 nM). These results confirm the direct regulatory role of RamR in the repression oframAtranscription and precisely define how an alteration of its binding site can give rise to an MDR phenotype.

scholarly journals Spatial Segregation of Virulence Gene Expression during Acute Enteric Infection with Salmonella enterica serovar Typhimurium

mBio ◽  
2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Richard C. Laughlin ◽  
Leigh A. Knodler ◽  
Roula Barhoumi ◽  
H. Ross Payne ◽  
Jing Wu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Salmonella Enterica ◽  
Virulence Gene ◽  
Bacterial Virulence ◽  
Natural Host ◽  
Host Cells ◽  
Enteric Infection ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Serovar Typhimurium

ABSTRACTTo establish a replicative niche during its infectious cycle between the intestinal lumen and tissue, the enteric pathogenSalmonella entericaserovar Typhimurium requires numerous virulence genes, including genes for two type III secretion systems (T3SS) and their cognate effectors. To better understand the host-pathogen relationship, including early infection dynamics and induction kinetics of the bacterial virulence program in the context of a natural host, we monitored the subcellular localization and temporal expression of T3SS-1 and T3SS-2 using fluorescent single-cell reporters in a bovine, ligated ileal loop model of infection. We observed that the majority of bacteria at 2 h postinfection are flagellated, express T3SS-1 but not T3SS-2, and are associated with the epithelium or with extruding enterocytes. In epithelial cells,S. Typhimurium cells were surrounded by intact vacuolar membranes or present within membrane-compromised vacuoles that typically contained numerous vesicular structures. By 8 h postinfection, T3SS-2-expressing bacteria were detected in the lamina propria and in the underlying mucosa, while T3SS-1-expressing bacteria were in the lumen. Our work identifies for the first time the temporal and spatial regulation of T3SS-1 and -2 expression during an enteric infection in a natural host and provides further support for the concept of cytosolicS. Typhimurium in extruding epithelium as a mechanism for reseeding the lumen.IMPORTANCEThe pathogenic bacteriumSalmonella entericaserovar Typhimurium invades and persists within host cells using distinct sets of virulence genes. Genes fromSalmonellapathogenicity island 1 (SPI-1) are used to initiate contact and facilitate uptake into nonphagocytic host cells, while genes within SPI-2 allow the pathogen to colonize host cells. While many studies have identified bacterial virulence determinants in animal models of infection, very few have focused on virulence gene expression at the single-cell level during anin vivoinfection. To better understand when and where bacterial virulence factors are expressed during an acute enteric infection of a natural host, we infected bovine jejunal-ileal loops withS. Typhimurium cells harboring fluorescent transcriptional reporters for SPI-1 and -2 (PinvFand PssaG, respectively). After a prescribed time of infection, tissue and luminal fluid were collected and analyzed by microscopy. During early infection (≤2 h), bacteria within both intact and compromised membrane-bound vacuoles were observed within the epithelium, with the majority expressing SPI-1. As the infection progressed,S. Typhimurium displayed differential expression of the SPI-1 and SPI-2 regulons, with the majority of tissue-associated bacteria expressing SPI-2 and the majority of lumen-associated bacteria expressing SPI-1. This underscores the finding thatSalmonellavirulence gene expression changes as the pathogen transitions from one anatomical location to the next.

scholarly journals Effects of Norspermidine and Spermidine on Biofilm Formation by Potentially Pathogenic Escherichia coli and Salmonella enterica Wild-Type Strains

2015 ◽  
Vol 81 (6) ◽  
pp. 2226-2232 ◽  
Author(s):  
Live L. Nesse ◽  
Kristin Berg ◽  
Lene K. Vestby
Keyword(s):  
Escherichia Coli ◽  
Salmonella Enterica ◽  
Biofilm Formation ◽  
Wild Type ◽  
Content Type ◽  
E Coli ◽  
Pathogenic Escherichia Coli ◽  
Serovar Typhimurium ◽  
And Control ◽  
Type Strains

ABSTRACTPolyamines are present in all living cells. In bacteria, polyamines are involved in a variety of functions, including biofilm formation, thus indicating that polyamines may have potential in the control of unwanted biofilm. In the present study, the effects of the polyamines norspermidine and spermidine on biofilms of 10 potentially pathogenic wild-type strains ofEscherichia coliserotype O103:H2,Salmonella entericasubsp.entericaserovar Typhimurium, andS. entericaserovar Agona were investigated. We found that exogenously supplied norspermidine and spermidine did not mediate disassembly of preformed biofilm of any of theE. coliandS. entericastrains. However, the polyamines did affect biofilm production. Interestingly, the two species reacted differently to the polyamines. Both polyamines reduced the amount of biofilm formed byE. colibut tended to increase biofilm formation byS. enterica. Whether the effects observed were due to the polyamines specifically targeting biofilm formation, being toxic for the cells, or maybe a combination of the two, is not known. However, there were no indications that the effect was mediated through binding to exopolysaccharides, as earlier suggested forE. coli. Our results indicate that norspermidine and spermidine do not have potential as inhibitors ofS. entericabiofilm. Furthermore, we found that the commercial polyamines used contributed to the higher pH of the test medium. Failure to acknowledge and control this important phenomenon may lead to misinterpretation of the results.

scholarly journals Two Tandem Mechanisms Control Bimodal Expression of the Flagellar Genes in Salmonella enterica

2020 ◽  
Vol 202 (13) ◽  
Author(s):  
Xiaoyi Wang ◽  
Santosh Koirala ◽  
Phillip D. Aldridge ◽  
Christopher V. Rao
Keyword(s):  
Gene Expression ◽  
Salmonella Enterica ◽  
Feedback Loop ◽  
Growth Conditions ◽  
Double Negative ◽  
Flagellar Gene ◽  
Content Type ◽  
Motile Cells ◽  
Flagellar Assembly ◽  
Flagellar Genes

ABSTRACT Flagellar gene expression is bimodal in Salmonella enterica. Under certain growth conditions, some cells express the flagellar genes whereas others do not. This results in mixed populations of motile and nonmotile cells. In the present study, we found that two independent mechanisms control bimodal expression of the flagellar genes. One was previously found to result from a double negative-feedback loop involving the flagellar regulators RflP and FliZ. This feedback loop governs bimodal expression of class 2 genes. In this work, a second mechanism was found to govern bimodal expression of class 3 genes. In particular, class 3 gene expression is still bimodal, even when class 2 gene expression is not. Using a combination of experimental and modeling approaches, we found that class 3 bimodality results from the σ28-FlgM developmental checkpoint. IMPORTANCE Many bacterial use flagella to swim in liquids and swarm over surface. In Salmonella enterica, over 50 genes are required to assemble flagella. The expression of these genes is tightly regulated. Previous studies have found that flagellar gene expression is bimodal in S. enterica, which means that only a fraction of cells express flagellar genes and are motile. In the present study, we found that two separate mechanisms induce this bimodal response. One mechanism, which was previously identified, tunes the fraction of motile cells in response to nutrients. The other results from a developmental checkpoint that couples flagellar gene expression to flagellar assembly. Collectively, these results further our understanding of how flagellar gene expression is regulated in S. enterica.

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