Fig 1.
(A) A putative quadruplex sequence (PQS) is a nucleotide sequence predicted to form a G4 structure. A degenerate PQS used to predict the formation of intramolecular G4s is shown here, consisting of four runs of at least three guanines per run, separated by short stretches of other bases (N). (B) The basic unit of the G4 is the G-tetrad. (C) G4 structures display a large variety of different topologies. Topology of intramolecular G4 structures displaying antiparallel (left) and parallel (right) configurations. (D) Topology of intermolecular G4 structures formed by dimerisation of four strands (left) or two strands (right).
Fig 2.
Schematic model of the role of the pilE G-quadruplex (G4) in N. gonorrhoeae pilin antigenic variation.
A putative quadruplex sequence (PQS) and a small RNA (sRNA) promoter are located upstream of the pilE locus (A). The initiation of transcription from the sRNA promoter (B) provides the single-stranded conditions required for G4 formation (C). The pilE G4 recruits RecA (D) and potentially other recombination factors, which stimulates non-reciprocal recombination between a pilS locus and the pilE locus (E).
Fig 3.
Schematic representation of the mechanisms by which G-quadruplexes (G4) may contribute to the maintenance of viral latency.
(A) In the integrated HIV-1 provirus, the U3 region contains two NF-κΒ binding sites (black blocks) and three Sp1 binding sites (grey blocks). Here, the formation of a G4 from the G-rich Sp1 binding sites is shown, but several distinct G4s can form in this region. G4 formation inhibits transcription from the transcription start site (TSS). This transcriptional repression may be mediated by the differential affinity of transcription factors for double-stranded and G4 DNA. (B) The glycine-alanine repeat domain of Epstein-Barr virus-encoded nuclear antigen 1 (EBNA1) mRNA contains PQS. G4 formation inhibits translation, thereby reducing EBNA1 protein levels and limiting the presentation of EBNA1 peptides by antigen presenting cells (APC) via the major histocompatibility complex (MHC) pathway.
Fig 4.
Phylogenetic tree schematic displaying the evolutionary relationships among the pathogens discussed in this review.
The model systems S. cerevisiae and E. coli are also shown. Branches are not proportional to evolutionary distance.
Table 1.
G-quadruplexes in pathogens.