Affinage · Toxoplasma gondii

TOM7

mitochondrial import receptor subunit TOM7 · UniProt S8G8T8

Annotated
2026-09-08
1 papers in source corpus 1 papers cited in narrative 2 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TgTom7 is a component of the translocon of the outer mitochondrial membrane (TOM) complex in Toxoplasma gondii that is required for parasite survival and mitochondrial protein import (PMID:27458014). Loss-of-function analysis establishes that TgTom7 is important for TOM complex stability, a role that diverges from its yeast ortholog, where Tom7 destabilizes the TOM complex — indicating functional divergence during eukaryotic evolution (PMID:27458014). Beyond these loss-of-function phenotypes, no further mechanistic detail has been characterized in the available corpus.

Mechanistic history

Synthesis pass · year-by-year structured walk · 2 steps
  1. 2016 Medium

    Whether the Toxoplasma Tom7 homologue contributes to parasite viability and mitochondrial biogenesis was unknown; loss-of-function analysis established that TgTom7 is required for parasite survival and mitochondrial protein import, defining it as a functionally important TOM component.

    Evidence Loss-of-function (knockdown/knockout) with readouts of parasite survival and mitochondrial protein import in T. gondii

    PMID:27458014

    Open questions at the time
    • Molecular mechanism of how TgTom7 supports protein import is not defined
    • Direct binding partners within the TOM complex not identified
    • Single lab, single study
  2. 2016 Medium

    Because yeast Tom7 destabilizes the TOM complex, whether the parasite ortholog retained this activity was unclear; complex-stability assays showed TgTom7 instead promotes TOM complex stability, establishing a diverged function during eukaryotic evolution.

    Evidence Loss-of-function analysis with assessment of TOM complex assembly/stability in T. gondii

    PMID:27458014

    Open questions at the time
    • Structural basis for the stabilizing versus destabilizing role not resolved
    • Whether stability defect fully accounts for the import defect is untested
    • No reciprocal validation across independent labs

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular basis by which TgTom7 stabilizes the TOM complex and enables protein import, including its direct partners and structural arrangement, remains unresolved.
  • No interaction map of TgTom7 within the TOM complex
  • No structural model
  • Substrate specificity of the import defect not characterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification
Complex memberships
TOM complex (translocon of the outer mitochondrial membrane)

Evidence

Reading pass · 2 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2016 TgTom7 (T. gondii homologue of Tom7) is important for parasite survival and mitochondrial protein import, as demonstrated by loss-of-function analysis. Loss-of-function (knockdown/knockout) with readout of parasite survival and mitochondrial protein import The Journal of biological chemistry Medium 27458014
2016 Contrary to the role of Tom7 in yeast (where it destabilizes the TOM complex), TgTom7 is important for TOM complex stability in T. gondii, indicating a diverged function during eukaryotic evolution. Loss-of-function analysis with assessment of TOM complex assembly/stability The Journal of biological chemistry Medium 27458014

Source papers

Stage 0 corpus · 1 paper · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 The Import of Proteins into the Mitochondrion of Toxoplasma gondii. The Journal of biological chemistry 42 27458014