Global Effect of E. Coli T3SS2 on Cell Surface and Pathogenicity

This report investigates the Escherichia coli Type III Secretion System 2 (ETT2) and its global effects on the bacterial cell surface. The study focuses on E. coli serotype O2, which possesses an intact ETT2 gene cluster. Through proteomic analysis, the research identifies that the ETT2 gene cluster does not secrete effectors. Instead, the majority of secreted proteins were identified as flagellar proteins. Deletion of the ETT2 gene cluster resulted in reduced secretion of flagellar proteins, altered surface properties, and effects on serum resistance. The study also explores the potential of targeting ETT2 to counter bacterial surface effects, and its crucial role in serum resistance, which is responsible for septicaemia. The report addresses questions on the effect of ETT2 resistance on bacterial pathogenicity, confounding factors affecting ETT2 sensitivity, and the impact of effector secretion on the ETT2 effect, highlighting the importance of virulence factors in ExPEC strains. The research concludes that the ETT2 gene cluster plays a significant role in the pathogen city and ability of bacterial survival on serum and sepsis occurrence.

Abstract
The Escherichia Coli Type III Secretion System 2 Has a Global
Effect on Cell Surface
Alexander Shulman,a,b Yael Yair, Dvora Biran, Thomas Sura, C,Andreas Otto,c Uri Gophna,a Dörte Becher,c Michael Hecker,cEliora Z. Ron
Introduction: Type III secretion system is an important factor for the deliverance of effector
proteins into host’s cells subverting host cellular processes. Enter pathogenic Eschericha Coli such
as O157 and T3SS exists in playing an essential role of attachment and effacement. E.Coli genomes
often appear in a similar cluster which resembles the pathogenicity island SP-1 system present in
Salmonella and encode the T3SS. The gene cluster present is ETT2 which is present in many E.
Coli strains and has large quantities of mutations, deletions and insertions. The ETT2 encodes the
secretion of cells thus enhancing effectors into the host cells. Changes on the structural forms of
ETT2 could play a significant factor in reducing manifestation and inability producing the needle of
the TSS apparatus. E Coli has ETT2 pathogenic island and don’t poses the enterocyte effacement. It
has the potential of encoding the secretion of the associated proteins. This experiment explored the
effectors proteins and its role on secretion system function. Methods and materials: E. Coli
serotype was isolated from the avian E. Coli septicaemia. Antibiotics were added with the required
concentrations. E Coli serotype was used for deletion of strains and complementing the plasmids,
utilizing competent and wild types. The serum was grown through overnight culture and diluted in
fresh medium until the desired growth density novobiocin resistance was cultured and stored, while
secrotome were collected using strata clean resin beds. Analysis was performed using proteomic
analysis, while motility assay were measured after culture dilution. The resulting RNA was isolated
and purified. Real time protein transcription was performed. Results: The ETT2 gene cluster of E.
Coli of 02 was found not to have any secretion effectors into the cells. Proteomic analysis of
proteome showed a cystolic fraction of the wild strains and substantial amounts occurring on FIgM
amount. Deletion of the ETT2 showed reduced expression of the flagella genes, further here was an
observed effect on the distribution of secretion fibril proteins. Further deleting the ETT2 gene
cluster changed the surface properties and effects on serum resistance. Discussions: The ETT2
changes has effects on proteins structure, its deletion effects synthesis rather than secretion and
being sensitive to mutants. Effects on ET2 gene cluster; an important factor on pathogen city and
ability of bacterial survival on serum and sepsis occurrence was noted. The ExPEC strains have an
effect on broad spectrum resistance and vaccine development. Virulence factors are key on this
strain. Targeting ETT2 is effective in countering bacterial surface, playing crucial role on serum
resistance responsible for septicaemia.
Questions: i) What is the effect of ETT2 resistance on bacterial pathogenic of host cells?
ii) What are other confounding factors having an effect on ETT2 sensitivity role?
iii) How does the secretion of injecting effectors in host cells affect the ETT2 effect?
Limitation :The ETT2 pathogen city only plays a significant role on Eschericha Coli specific sites
thus limiting its pathogenic effect.