transposable element

traitmech:000092 · CLASS · REVIEWED

A genomics trait describing possession of transposable elements — such as insertion sequences and transposons — that move within the genome and drive genome rearrangement, gene inactivation, and plasticity.

Transposable elements drive DNA transposition and genome rearrangement

Evidence-backed causal sketch linking TE possession to DNA transposition activity and resulting genome rearrangement and plasticity.

Transposable elements drive DNA transposition and genome rearrangement Interactive directed graph showing evidence-backed causal relationships for transposable element.

Edge evidence

  • transposable element enables DNA transposition RO:0002327

    TEs encode transposases that catalyze transposition.

    • DOI:10.1111/1574-6976.12067 Siguier et al. review insertion-sequence transposase machinery and activity.
  • DNA transposition causes genome rearrangement biolink:causes

    Transposition events generate insertions and rearrangements.

    • DOI:10.1038/nrmicro1235 Frost et al. cite transposons among MGEs driving genome evolution.
  • transposable element has participant transposase

    The defining effector of a TE is a transposase required for movement.

    • DOI:10.1128/MMBR.00119-22 IS element encodes a single ORF, a DDE-family transposase required for movement (Harmer & Hall 2024).
  • transposase enables DNA transposition RO:0002327

    Transposase activity is causal for element movement/transposition.

    • DOI:10.1128/MMBR.00119-22 tnp26 encodes a transposase required for movement (Harmer & Hall 2024).
  • transposable element insertion causes target site duplication biolink:causes

    Element insertion typically generates short flanking target site duplications.

    • DOI:10.1038/s41467-023-39964-7 Insertion sequences typically create target site duplications (TSDs) upon insertion (Sheng et al. 2023).
  • transposable element insertion causes gene disruption biolink:causes

    Insertion into a coding region disrupts gene function.

    • DOI:10.1038/s41467-023-39964-7 Element movement causes gene disruption (Sheng et al. 2023).
  • homologous recombination between IS copies causes genome rearrangement biolink:causes

    Recombination between identical IS copies produces genome rearrangements.

    • DOI:10.1038/s41467-023-39964-7 Homologous recombination between identical IS copies can produce genome rearrangements (Sheng et al. 2023).

Provenance

Source
METPO (2025-11-25)
Definition source
DOI:10.1111/1574-6976.12067

Synonyms (2)

  • insertion sequence RELATED_SYNONYM · DOI:10.1111/1574-6976.12067
  • transposon RELATED_SYNONYM · DOI:10.1111/1574-6976.12067

kg-microbe context

Matched 1 kg-microbe node via parent_proxy.

  • METPO:1000188 [-0.956, -1.962, -3.148, +1.274, …]

512-dim DeepWalkSkipGramEnsmallen embedding from kg-microbe (2026-04-25).

Nearest neighbors in embedding space

Top-8 cosine-similar METPO traits from the 2026-04-25 deepwalk (512-D).

Deep research

Generated by just research-trait; source: research/traits/genomics/transposable_element-deep-research-falcon.md

Unreviewed literature output — not curated TraitMech content Ontology identifiers suggested below have not been resolved against their ontologies, and some are known to be wrong. Check any CURIE against the source before using it.
# Curation report: microbial transposable element

**Trait:** `traitmech:000092`  
**Category:** GENOMICS | **Term kind:** CLASS | **Mapping:** REVIEWED  
**Parent:** `traitmech:000089`

## 1. Scope summary

This trait should mean **genomic possession of at least one transposable element (TE)**: a DNA segment capable of changing genomic location through element-encoded or trans-supplied transposition machinery. In prokaryotes, an insertion sequence (IS) is the simplest autonomous form—typically a transposase ORF bounded by cognate ends—whereas larger or composite transposons may additionally carry “passenger” genes such as antimicrobial-resistance determinants. Nonautonomous elements belong in scope when recognizable as transposase-mobilizable TE derivatives. (hickman2016dnatranspositionat pages 2-3, siguier2014bacterialinsertionsequences pages 12-13)

The trait records **possession**, not necessarily current transposition activity. A defective or transcriptionally silent TE can therefore satisfy the trait, while an assay showing transposition rate is a related but different phenotype. Likewise, Tn-seq libraries made by experimentally delivering engineered Tn5/Mariner elements do not establish that the tested wild-type strain naturally possesses a TE. Modern Tn-seq constructs commonly place transposase outside the inserted segment to prevent remobilization. (fernandezgarcia2024essentialgenesdiscovery pages 2-4, fernandezgarcia2024essentialgenesdiscovery pages 1-2)

### Boundary cases

- **Include:** autonomous ISs; simple and composite transposons; replicative transposons; mobilizable nonautonomous TE derivatives; chromosomal or plasmid-borne elements.
- **Do not equate with:** plasmid possession, integron possession, prophage, integrative/conjugative elements, or horizontal gene transfer generally. These entities can carry or interact with TEs but have distinct replication/transfer machinery.
- **Do not require:** a resistance gene, terminal inverted repeats, target-site duplication, or a cut-and-paste mechanism. These are common but not universal. HUH-family elements use different chemistry, and some “peel-and-paste” systems do not produce target-site duplications. (hickman2016dnatranspositionat pages 5-6, tenjocastano2022transposonsandcrispr pages 2-3)
- **Assay caution:** a transposase annotation alone is suggestive, but fragmented assemblies and domesticated transposases can produce false-positive trait calls. Prefer a bounded element architecture, family assignment, or insertion evidence.

## 2. Current mechanistic model

The most defensible generic causal chain is:

**TE DNA containing cognate ends → transposase binding → end cleavage/excision or replicative strand transfer → target-DNA capture and integration → gap repair/target-site duplication where applicable → insertional mutation, altered neighboring-gene expression, or genome rearrangement → genomic plasticity.**

Transposases are site-specific endonucleases for their own element ends but are often less sequence-specific toward target DNA. In canonical DDE systems, acidic active-site residues coordinate divalent metal ions; exposed 3′-OH groups then attack target-DNA phosphodiester bonds. (hickman2016dnatranspositionat pages 3-5)

Mechanistic branching is essential. Cut-and-paste systems excise the donor copy; copy-in/replicative systems retain and duplicate it; copy-out–paste-in pathways pass through circular intermediates. IS200/IS605- and IS91-related HUH transposases instead use single-stranded intermediates and covalent 5′-phosphotyrosine linkages. (hickman2016dnatranspositionat pages 5-6, hickman2016dnatranspositionat pages 2-3)

For Tn3-family replicative transposition, transposase nicks both 3′ ends, the resulting 3′-OH groups attack staggered target strands, and repair of 5-bp gaps generates 5-bp direct target-site duplications in the cointegrate. This exact duplication length is family-specific and must not be generalized to all TEs. (nicolas2015thetn3familyof pages 13-15)

## 3. Candidate nodes grouped by type

### A. Trait and element-architecture nodes

- `traitmech:000092` — transposable element possession
- insertion sequence; simple transposon; composite transposon
- autonomous TE; nonautonomous TE
- transposon left end/right end
- terminal inverted repeat
- passenger gene/cargo DNA
- target-site duplication

These architecture nodes should remain **label-only** unless the project has verified ontology terms. ISfinder is the relevant specialist nomenclature resource; one review reported more than 4,000 classified IS sequences and about 30 recognized prokaryotic IS families at that time. (hickman2016dnatranspositionat pages 5-6)

### B. Genes, proteins, and complexes

- **transposase** — DDE/DD(E/D) or HUH catalytic class
- transpososome/synaptic complex
- **TnpR/resolvase** — family-scoped for cointegrate resolution
- H-NS, histone-like nucleoid-structuring protein
- TnsA, TnsB, TnsC, TnsD/TniQ and Cascade/Cas effector—only for Tn7/CAST branches
- IS-excision enhancer (IEE)—IS629-specific modifier

Recommended ontology-grounding candidates, subject to release-level verification, are **GO:0004803, transposase activity**, **GO:0006313, transposition, DNA-mediated**, and **GO:0003677, DNA binding**. Do not assign a generic transposase UniProt accession because transposases are element- and taxon-specific.

### C. Molecular intermediates and chemicals

- donor DNA and target DNA
- cleaved transposon-end 3′-OH

Showing the first 60 of 246 lines of findings; the linked file also carries the run's front matter and the prompt it was given — read the full report.

Curation history

  1. · PROPOSED_FROM_RESEARCH · claude

    Proposed candidate GENOMICS trait (transposable element); sub-variant of mobile genetic element.

  2. · CURATED_CAUSAL_GRAPH · claude

    Added evidence-backed causal graph (transposition / genome rearrangement) with GO node grounding and RO/biolink predicate groundings; promoted PROPOSED to REVIEWED.

  3. · ENRICH_CAUSAL_GRAPH · claude

    Added 5 evidence-backed generic edges (5 new nodes) from the deep-research report.

  4. · GROUND_CAUSAL_PREDICATES · claude

    Grounded 4 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (biolink:causes×3, RO:0002327×1).

  5. · GROUND_CAUSAL_NODES · claude

    Grounded 1 causal-node grounding field(s) via mappings/node_grounding.tsv (UniProtKB:A0A023WVD3×1).

  6. · RETRACT_DEAD_UNIPROT_GROUNDINGS · claude

    Retracted 1 UniProtKB grounding(s) whose accessions are deleted from UniProt; nodes demoted to label-only pending re-grounding (docs/GROUNDING_POLICY.md)

  7. · GROUND_CAUSAL_NODES · claude

    Grounded 1 causal-node grounding field(s) via mappings/node_grounding.tsv (GO:0004803×1).