Host–pathogen
How open is the Listeria pan-genome?
Open access · cc by · source: Europe PMC
Eleven new genomes spanning serotypes show a stable but open pan-genome with nine hypervariable hotspots dominated by mobile elements.
Study at a glance
- Design
- Computational / modelling — Extended L. monocytogenes complete-genome set covering all serotypes for pan-genome analysis
- N
- N=16 · 16 completely sequenced chromosomes (extended by 11 strains in this work)
- Population
- Listeria monocytogenes genomes across serotypes
- Outcome
- Pan-genome stability and accessory-gene hotspot dynamics
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
The pan-genome is highly stable but not closed; accessory genes concentrate in hypervariable hotspots with mobile genetic elements as major accessory components.
Methodology
Extended L. monocytogenes genome sets by 11 strains covering all serotypes and reassessed pan-genome structure.
Limitations
Gene presence/absence aids diagnostics/phylogenetics but does not alone prove each virulence phenotype.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
The pan-genome is highly stable but not closed; accessory genes concentrate in hypervariable hotspots with mobile genetic elements as major accessory components.
Evidence for the claim as stated.
Aspergillus clade genomics and a Listeria pan-genome reassessment use trees and gene-content matrices together. Aspergillus genomes were ~29–36 Mb with 9,113–13,553 genes, about 20% Aspergillaceae-specific, and section Nigri averaged ~1,800 unique genes. Extending L. monocytogenes by 11 strains covering all serotypes showed a highly stable but not closed pan-genome, with accessory genes in hypervariable hotspots and mobile elements as major accessory components.
Evidence for the claim as stated.
These papers do not build the same kind of tree. HSP90 and MYB papers classify gene families; the immune-gene paper scans orthologs for repeated positive selection (~14% selected in all tests); Aspergillus and Listeria papers mix clade phylogeny with pan-genome gene content; turtle and Medicago papers are organismal genomes whose phylogeny is background for physiology or breeding. A student who treats every 'phylogenetic analysis' hit as a species tree will misread the result.
Evidence for the claim as stated.
What 'accessory' or 'lineage-specific' genes imply is itself unsettled. Listeria accessory genes concentrate in hotspots with mobile elements and aid diagnostics, but presence/absence does not prove each virulence phenotype. Aspergillus section Nigri's ~1,800 unique genes are not experimentally validated one by one. Immune-gene sharing of selection between birds and mammals can be convergence or ancient pressure.
Evidence for the claim as stated.
Many papers in the CRISPR index mention CRISPR or Cas proteins in passing while the actual experiment is something else (APEX2 proximity labelling, pan-genome presence/absence, ChIP-seq of histone acylations, scRNA-seq of endoderm). Those hits show why a body-count lexicon over-recruits; they are not additional editing results.
Evidence for the claim as stated.
The strongest tension is naming. The 2007 array paper and the Listeria pan-genome treat CRISPR as a genomic feature of bacteria; the Cas13a and dCas9 papers treat CRISPR–Cas as a laboratory tool. Both usages are historically connected, but a finding about repeat RNA folding does not license a claim about editing a human promoter, and a CasIP result does not catalogue environmental CRISPR diversity.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
These papers do not build the same kind of tree. HSP90 and MYB papers classify gene families; the immune-gene paper scans orthologs for repeated positive selection (~14% selected in all tests); Aspergillus and Listeria papers mix clade phylogeny with pan-genome gene content; turtle and Medicago papers are organismal genomes whose phylogeny is background for physiology or breeding. A student who treats every 'phylogenetic analysis' hit as a species tree will misread the result.
- Supports · HSP90 family across kingdoms
- Supports · MYB transcription-factor families in plants
- Supports · Why do immune genes keep evolving across tetrapods?
What 'accessory' or 'lineage-specific' genes imply is itself unsettled. Listeria accessory genes concentrate in hotspots with mobile elements and aid diagnostics, but presence/absence does not prove each virulence phenotype. Aspergillus section Nigri's ~1,800 unique genes are not experimentally validated one by one. Immune-gene sharing of selection between birds and mammals can be convergence or ancient pressure.
- Supports · Aspergillus genomic diversity
- Supports · Why do immune genes keep evolving across tetrapods?
The strongest tension is naming. The 2007 array paper and the Listeria pan-genome treat CRISPR as a genomic feature of bacteria; the Cas13a and dCas9 papers treat CRISPR–Cas as a laboratory tool. Both usages are historically connected, but a finding about repeat RNA folding does not license a claim about editing a human promoter, and a CasIP result does not catalogue environmental CRISPR diversity.
- Supports · CRISPR repeats conserve RNA-like structure
- Supports · Can Cas13a fight RNA viruses in plants?
- Supports · FLI1 circRNA FECR1 drives metastasis
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