The type III protein secretion system contributes to Xanthomonas citri subsp. citri biofilm formation

Zimaro, Tamara; Thomas, Ludivine; Marondedze, Claudius; Sgro, Germán G.; Garofalo, Cecilia; Ficarra, Florencia A.; Gehring, Chris; Ottado, Jorgelina; Gottig, Natalia

doi:10.1186/1471-2180-14-96

Cited by 43 publications

(47 citation statements)

References 55 publications

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“…Notably, the ability of X. citri subsp. citri to form biofilms on abiotic surfaces, but not on plant tissue, is compromised by mutations in the type III secretion genes hrpB, hrpD, and hrpF (Zimaro et al, 2014). These observations suggest that E. psidii may require special conditions, probably mimicking the plant environ- of gene groups are predicted to be missing in the E. psidii strain IBSBF 435 draft genome (Hermenegildo et al, 2019), the absence of the investigated genes must be confirmed.…”

Section: Discussionmentioning

confidence: 96%

“…Notably, the ability of X. citri subsp. citri to form biofilms on abiotic surfaces, but not on plant tissue, is compromised by mutations in the type III secretion genes hrpB , hrpD , and hrpF (Zimaro et al , ). These observations suggest that E. psidii may require special conditions, probably mimicking the plant environment, for biofilm formation.…”

Section: Discussionmentioning

confidence: 99%

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Bidirectional colonization and biofilm formation by Erwinia psidii in eucalypt plants

et al. 2020

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Dieback and wilt caused by Erwinia psidii is an emerging disease that has been causing considerable damage in eucalypt plantations. Because it is a recently emerged disease, several aspects of the bacterial interaction with its host still remain to be elucidated. In this work, we studied the E. psidii colonization and biofilm formation in eucalypt tissues by specific detection using PCR and scanning electron microscopy (SEM). The results indicate that the bacterium is able to translocate in stem tissue mainly acropetally, although movement in the basipetal direction was also observed to a lesser extent, always through the xylem. No colonization of phloem tissues was observed. In addition to colonizing the xylem, E. psidii colonized the parenchymatous tissue. The bacterium formed cell aggregates enveloped by fibrillar material that evolved into complex, well‐structured biofilms in stem and leaf tissues. In contrast, no biofilm formation was observed on abiotic surfaces. These observations suggest that biofilm formation plays an important role in the elicitation of dieback and wilt symptoms caused by E. psidii on eucalypt plants. This study not only shows ultrastructural aspects of the E. psidii communities but also tissue damage in eucalypt plants that was associated with the presence of bacterial aggregates and formation of tyloses.

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Section: Discussionmentioning

confidence: 96%

“…Notably, the ability of X. citri subsp. citri to form biofilms on abiotic surfaces, but not on plant tissue, is compromised by mutations in the type III secretion genes hrpB , hrpD , and hrpF (Zimaro et al , ). These observations suggest that E. psidii may require special conditions, probably mimicking the plant environment, for biofilm formation.…”

Section: Discussionmentioning

confidence: 99%

Bidirectional colonization and biofilm formation by Erwinia psidii in eucalypt plants

et al. 2020

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“…Given the observed differences in bacterial adherence to PVC and glass surfaces, we tested whether XccΔoprB shows impaired ability to adhere to the leaf surface, using CV staining to measure bacterial attachment. Xcc and XccΔoprBc were able to adhere to the leaf tissue, as observed previously for the wild‐type strain (Zimaro et al ., ), whereas the XccΔoprB mutant could not adhere, shown by the absence of CV staining (Fig. A,B).…”

Section: Resultsmentioning

confidence: 95%

“…This may be attributed to the fact that the lack of biofilm formation in the mutant strain probably triggers a deregulation of xanthan production, given that gumD expression is also increased in the mutant strain in order to compensate for the lack of the aggregative state. This has been observed previously in another Xcc mutant strain which was unable to form a biofilm, but showed increased xanthan production, as well as XanA and GalU overexpression, compared with Xcc wild‐type (Zimaro et al ., ), and also in an Xcc adhesin deletion mutant (Gottig et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Xanthomonas citri ssp. citri requires the outer membrane porin OprB for maximal virulence and biofilm formation

Ficarra

Grandellis

Galván

et al. 2016

Molecular Plant Pathology

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Xanthomonas citri ssp. citri (Xcc) causes canker disease in citrus, and biofilm formation is critical for the disease cycle. OprB (Outer membrane protein B) has been shown previously to be more abundant in Xcc biofilms compared with the planktonic state. In this work, we showed that the loss of OprB in an oprB mutant abolishes bacterial biofilm formation and adherence to the host, and also compromises virulence and efficient epiphytic survival of the bacteria. Moreover, the oprB mutant is impaired in bacterial stress resistance. OprB belongs to a family of carbohydrate transport proteins, and the uptake of glucose is decreased in the mutant strain, indicating that OprB transports glucose. Loss of OprB leads to increased production of xanthan exopolysaccharide, and the carbohydrate intermediates of xanthan biosynthesis are also elevated in the mutant. The xanthan produced by the mutant has a higher viscosity and, unlike wild-type xanthan, completely lacks pyruvylation. Overall, these results suggest that Xcc reprogrammes its carbon metabolism when it senses a shortage of glucose input. The participation of OprB in the process of biofilm formation and virulence, as well as in metabolic changes to redirect the carbon flux, is discussed. Our results demonstrate the importance of environmental nutrient supply and glucose uptake via OprB for Xcc virulence.

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“…For instance, the T3SS of the phytopathogen Xanthomonas citri subsp. citri is necessary for biofilm formation (21), and hyperactivity of the T3SS encoded by Salmonella pathogenicity island 1(SPI1) can mediate biofilm-like cell aggregation (22). Biofilms, highly structured microbial communities featuring bacterial cells attaching to a biotic or abiotic surface and embedded in a matrix (23,24), may neutralize the conventional antimicrobial effect and host defense and thus are difficult to eradicate (25).…”

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confidence: 99%

Type III Secretion System Translocon Component EseB Forms Filaments on and Mediates Autoaggregation of and Biofilm Formation by Edwardsiella tarda

Gao

Nie

et al. 2015

Appl Environ Microbiol

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The type III secretion system (T3SS) of Edwardsiella tarda plays an important role in infection by translocating effector proteins into host cells. EseB, a component required for effector translocation, is reported to mediate autoaggregation of E. tarda. In this study, we demonstrate that EseB forms filamentous appendages on the surface of E. tarda and is required for biofilm formation by E. tarda in Dulbecco's modified Eagle's medium (DMEM). Biofilm formation by E. tarda in DMEM does not require FlhB, an essential component for assembling flagella. Dynamic analysis of EseB filament formation, autoaggregation, and biofilm formation shows that the formation of EseB filaments occurs prior to autoaggregation and biofilm formation. The addition of an EseB antibody to E. tarda cultures before bacterial autoaggregation prevents autoaggregation and biofilm formation in a dose-dependent manner, whereas the addition of the EseB antibody to E. tarda cultures in which biofilm is already formed does not destroy the biofilm. Therefore, EseB filament-mediated bacterial cell-cell interaction is a prerequisite for autoaggregation and biofilm formation. Edwardsiella tarda is a Gram-negative bacterium with a wide range of hosts, including fish and humans. E. tarda causes hemorrhagic septicemia in fish and gastrointestinal and extraintestinal infections in humans (1-3). The type III secretion system (T3SS) of E. tarda plays a pivotal role in infection and enables the bacteria to survive and replicate in phagocytes and epithelial cells (4-7).The bacterial T3SS nanomachine, delivering effector proteins directly from the bacterial cytosol to host cells (8, 9), consists of three parts: the basal body, needle, and translocation pore (10). The gene cluster of the T3SS in E. tarda contains 34 genes, which encode secretion apparatus, chaperones, translocators, effectors, and regulators (5, 11). The esrA-esrB (5) and esrC (12) genes in the T3SS gene cluster together with phoP-phoQ (13) and phoB-phoR (14) outside the T3SS gene cluster control the virulence of E. tarda. Deletion of esrB abolished the secretion of the translocon proteins EseB, EseC, and EseD (5), which can form a protein complex after secretion (5, 15, 16). Mutation of eseB led to an E. tarda replication defect in host cells (5). EseB is required not only for translocating effectors into host cells (11) but also for bacterial autoaggregation in a T3SS-inducing medium, Dulbecco's modified Eagle's medium (DMEM) (5).EseB is homologous to EspA of enteropathogenic Escherichia coli (EPEC) or enterohemorrhagic Escherichia coli (EHEC), and it has been reported that EspA forms a sheath-like structure on the bacterial surface, as revealed by immunofluorescent staining and immunogold labeling, and is required for effector translocation (17-19). EspA of EPEC or EHEC also functions as an adhesin in microcolony formation on epithelial cells and is involved in bacterial aggregation during biofilm formation on abiotic surfaces or salad leaves (19,20). The contribution of the T3SS to biofilm ...

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The type III protein secretion system contributes to Xanthomonas citri subsp. citri biofilm formation

Cited by 43 publications

References 55 publications

Bidirectional colonization and biofilm formation by Erwinia psidii in eucalypt plants

Bidirectional colonization and biofilm formation by Erwinia psidii in eucalypt plants

Xanthomonas citri ssp. citri requires the outer membrane porin OprB for maximal virulence and biofilm formation

Type III Secretion System Translocon Component EseB Forms Filaments on and Mediates Autoaggregation of and Biofilm Formation by Edwardsiella tarda

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