Format

Send to

Choose Destination
EcoSal Plus. 2016 Oct;7(1). doi: 10.1128/ecosalplus.ESP-0020-2015.

The Mosaic Type IV Secretion Systems.

Author information

1
Department of Microbiology and Molecular Genetics, The University of Texas Medical School at Houston, Houston, TX 77030.

Abstract

Escherichia coli and other Gram-negative and -positive bacteria employ type IV secretion systems (T4SSs) to translocate DNA and protein substrates, generally by contact-dependent mechanisms, to other cells. The T4SSs functionally encompass two major subfamilies, the conjugation systems and the effector translocators. The conjugation systems are responsible for interbacterial transfer of antibiotic resistance genes, virulence determinants, and genes encoding other traits of potential benefit to the bacterial host. The effector translocators are used by many Gram-negative pathogens for delivery of potentially hundreds of virulence proteins termed effectors to eukaryotic cells during infection. In E. coli and other species of Enterobacteriaceae, T4SSs identified to date function exclusively in conjugative DNA transfer. In these species, the plasmid-encoded systems can be classified as the P, F, and I types. The P-type systems are the simplest in terms of subunit composition and architecture, and members of this subfamily share features in common with the paradigmatic Agrobacterium tumefaciens VirB/VirD4 T4SS. This review will summarize our current knowledge of the E. coli systems and the A. tumefaciens P-type system, with emphasis on the structural diversity of the T4SSs. Ancestral P-, F-, and I-type systems were adapted throughout evolution to yield the extant effector translocators, and information about well-characterized effector translocators also is included to further illustrate the adaptive and mosaic nature of these highly versatile machines.

PMID:
27735785
PMCID:
PMC5119655
DOI:
10.1128/ecosalplus.ESP-0020-2015
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Ingenta plc Icon for PubMed Central
Loading ...
Support Center