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Highly recombinant VGII Cryptococcus gattii population develops clonal outbreak clusters through both sexual macroevolution and asexual microevolution.

Billmyre RB, Croll D, Li W, Mieczkowski P, Carter DA, Cuomo CA, Kronstad JW, Heitman J - MBio (2014)

Bottom Line: We found that VGIIa/b/c populations show evidence of clonal expansion in the PNW.We also found that the genomes of two basal VGII isolates from HIV(+) patients contain an introgression tract spanning three genes.This work shows that multiple processes can contribute to the emergence of an outbreak.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, USA heitm001@duke.edu.

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Related in: MedlinePlus

Genomic islands of high polymorphism on supercontig 13 are caused by two distinct VGII clades. (A) Linkage disequilibria (R2) among SNP loci on supercontig 13. Two regions located between positions 393 and 417 kb were in high linkage disequilibria. (B) Polymorphism among VGII isolates on supercontig 13. An island of high polymorphism colocalized with high linkage disequilibria between positions 393 and 417 kb. (C) The islands of high polymorphism were caused by the presence of two distinct groups of VGII isolates. Exclusion of isolates 2001/935-1 and IP96/1120-1 reduced the polymorphism within VGII to low levels (red area) between positions 393 and 408 kb compared to polymorphism among all VGII isolates (gray area). Exclusion of isolates NT3, NT7, NT8, RDH2, RDH7, and MMRL2647 reduced the polymorphism within VGII to low levels (blue area) between positions 414 and 417 kb compared to polymorphism among all VGII isolates (gray area). (D) Maximum likelihood phylogeny of VGII isolates based on all SNP on supercontig 13. Values indicate bootstrap support among 100 replicates. Isolates 2001/935-1 and IP96/1120-1 and isolates NT3, NT7, NT8, RDH2, RDH7, and MMRL2647 each grouped into a distinct clade of VGII.
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fig8: Genomic islands of high polymorphism on supercontig 13 are caused by two distinct VGII clades. (A) Linkage disequilibria (R2) among SNP loci on supercontig 13. Two regions located between positions 393 and 417 kb were in high linkage disequilibria. (B) Polymorphism among VGII isolates on supercontig 13. An island of high polymorphism colocalized with high linkage disequilibria between positions 393 and 417 kb. (C) The islands of high polymorphism were caused by the presence of two distinct groups of VGII isolates. Exclusion of isolates 2001/935-1 and IP96/1120-1 reduced the polymorphism within VGII to low levels (red area) between positions 393 and 408 kb compared to polymorphism among all VGII isolates (gray area). Exclusion of isolates NT3, NT7, NT8, RDH2, RDH7, and MMRL2647 reduced the polymorphism within VGII to low levels (blue area) between positions 414 and 417 kb compared to polymorphism among all VGII isolates (gray area). (D) Maximum likelihood phylogeny of VGII isolates based on all SNP on supercontig 13. Values indicate bootstrap support among 100 replicates. Isolates 2001/935-1 and IP96/1120-1 and isolates NT3, NT7, NT8, RDH2, RDH7, and MMRL2647 each grouped into a distinct clade of VGII.

Mentions: Polymorphisms among VGII isolates are not homogeneous along the chromosomes. In contrast with the islands of diminished polymorphism, we found SNP density was elevated locally, resulting in genomic islands of high polymorphism. For example, a region on R265 supercontig 13 located between 393 and 417 kb showed 3× to 4× more polymorphisms than the surrounding regions (Fig. 8B). This region coincides with two blocks of high linkage disequilibrium on supercontig 13 (Fig. 8A). We examined whether the increased polymorphisms were caused by the inclusion of particular VGII isolates and found that the high polymorphisms between positions 393 and 408 kb are caused by two outlying clonally related isolates (2001/935-1 and IP96/1120-1) (Fig. 8D). Removal of these two isolates reduced the polymorphism to levels identical to the genomic surroundings (red area in Fig. 8C). Similarly, the high level of polymorphism in the region from 414 to 417 kb is caused by the presence of six clonal isolates from the VGIInt group (NT3, NT7, NT8, RDH2, RDH7, and MMRL2647) (Fig. 8D). Removal of these six isolates from the analysis drastically reduced the level of polymorphism in this region (blue area in Fig. 8C).


Highly recombinant VGII Cryptococcus gattii population develops clonal outbreak clusters through both sexual macroevolution and asexual microevolution.

Billmyre RB, Croll D, Li W, Mieczkowski P, Carter DA, Cuomo CA, Kronstad JW, Heitman J - MBio (2014)

Genomic islands of high polymorphism on supercontig 13 are caused by two distinct VGII clades. (A) Linkage disequilibria (R2) among SNP loci on supercontig 13. Two regions located between positions 393 and 417 kb were in high linkage disequilibria. (B) Polymorphism among VGII isolates on supercontig 13. An island of high polymorphism colocalized with high linkage disequilibria between positions 393 and 417 kb. (C) The islands of high polymorphism were caused by the presence of two distinct groups of VGII isolates. Exclusion of isolates 2001/935-1 and IP96/1120-1 reduced the polymorphism within VGII to low levels (red area) between positions 393 and 408 kb compared to polymorphism among all VGII isolates (gray area). Exclusion of isolates NT3, NT7, NT8, RDH2, RDH7, and MMRL2647 reduced the polymorphism within VGII to low levels (blue area) between positions 414 and 417 kb compared to polymorphism among all VGII isolates (gray area). (D) Maximum likelihood phylogeny of VGII isolates based on all SNP on supercontig 13. Values indicate bootstrap support among 100 replicates. Isolates 2001/935-1 and IP96/1120-1 and isolates NT3, NT7, NT8, RDH2, RDH7, and MMRL2647 each grouped into a distinct clade of VGII.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig8: Genomic islands of high polymorphism on supercontig 13 are caused by two distinct VGII clades. (A) Linkage disequilibria (R2) among SNP loci on supercontig 13. Two regions located between positions 393 and 417 kb were in high linkage disequilibria. (B) Polymorphism among VGII isolates on supercontig 13. An island of high polymorphism colocalized with high linkage disequilibria between positions 393 and 417 kb. (C) The islands of high polymorphism were caused by the presence of two distinct groups of VGII isolates. Exclusion of isolates 2001/935-1 and IP96/1120-1 reduced the polymorphism within VGII to low levels (red area) between positions 393 and 408 kb compared to polymorphism among all VGII isolates (gray area). Exclusion of isolates NT3, NT7, NT8, RDH2, RDH7, and MMRL2647 reduced the polymorphism within VGII to low levels (blue area) between positions 414 and 417 kb compared to polymorphism among all VGII isolates (gray area). (D) Maximum likelihood phylogeny of VGII isolates based on all SNP on supercontig 13. Values indicate bootstrap support among 100 replicates. Isolates 2001/935-1 and IP96/1120-1 and isolates NT3, NT7, NT8, RDH2, RDH7, and MMRL2647 each grouped into a distinct clade of VGII.
Mentions: Polymorphisms among VGII isolates are not homogeneous along the chromosomes. In contrast with the islands of diminished polymorphism, we found SNP density was elevated locally, resulting in genomic islands of high polymorphism. For example, a region on R265 supercontig 13 located between 393 and 417 kb showed 3× to 4× more polymorphisms than the surrounding regions (Fig. 8B). This region coincides with two blocks of high linkage disequilibrium on supercontig 13 (Fig. 8A). We examined whether the increased polymorphisms were caused by the inclusion of particular VGII isolates and found that the high polymorphisms between positions 393 and 408 kb are caused by two outlying clonally related isolates (2001/935-1 and IP96/1120-1) (Fig. 8D). Removal of these two isolates reduced the polymorphism to levels identical to the genomic surroundings (red area in Fig. 8C). Similarly, the high level of polymorphism in the region from 414 to 417 kb is caused by the presence of six clonal isolates from the VGIInt group (NT3, NT7, NT8, RDH2, RDH7, and MMRL2647) (Fig. 8D). Removal of these six isolates from the analysis drastically reduced the level of polymorphism in this region (blue area in Fig. 8C).

Bottom Line: We found that VGIIa/b/c populations show evidence of clonal expansion in the PNW.We also found that the genomes of two basal VGII isolates from HIV(+) patients contain an introgression tract spanning three genes.This work shows that multiple processes can contribute to the emergence of an outbreak.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, USA heitm001@duke.edu.

Show MeSH
Related in: MedlinePlus