Affinage · Toxoplasma gondii

RAB2

putative small GTPase Rab2 · UniProt A0A125YL14

Annotated
2026-09-08
3 papers in source corpus 3 papers cited in narrative 3 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

Toxoplasma gondii Rab2 is a Rab GTPase that functions in early secretory and vesicular trafficking, specifically the ER-to-Golgi transport pathway (PMID:38713739, PMID:37398139). Its GTPase cycle is controlled by TgTBC9, a protozoan-specific TBC domain-containing GTPase-activating protein (GAP) localized to the endoplasmic reticulum, which preferentially and directly binds Rab2 and requires the conserved dual-finger active site of its TBC domain for GAP activity (PMID:38713739). Loss of TgTBC9 disrupts ER and Golgi organization, consistent with dysregulated Rab2 at this trafficking step (PMID:38713739, PMID:37398139), and TBC9 additionally engages Rab11A and Rab11B, linking this regulatory node to daughter inner membrane complex (IMC) formation (PMID:38762629). Beyond its regulation by TgTBC9 in the secretory pathway, no further mechanistic detail on Rab2 effectors, nucleotide-exchange factors, or trafficking cargo has been characterized in the available corpus.

Mechanistic history

Synthesis pass · year-by-year structured walk · 3 steps
  1. 2023 Medium

    It was unknown which regulator controls the Rab2 GTPase cycle in Toxoplasma; identifying a direct binding partner established TgTBC9 as a candidate GAP governing ER-to-Golgi traffic.

    Evidence Immunoprecipitation and yeast two-hybrid binding plus auxin-inducible degron knockdown with fluorescence localization in T. gondii (preprint)

    PMID:37398139

    Open questions at the time
    • Preprint version later peer-reviewed
    • Catalytic GAP requirement not yet demonstrated at this stage
    • Effect on Rab2 nucleotide state not directly measured
  2. 2024 High

    Whether TgTBC9 acts catalytically on Rab2 rather than merely binding it was unresolved; active-site mutagenesis showed the conserved dual-finger motif is required for GAP function, establishing TgTBC9 as a bona fide Rab2 GAP controlling ER morphology and vesicular trafficking.

    Evidence Reciprocal Co-IP and yeast two-hybrid binding, auxin-inducible degron knockdown, and dual-finger active-site mutagenesis in T. gondii

    PMID:38713739

    Open questions at the time
    • Direct measurement of Rab2 GTP hydrolysis acceleration in vitro not reported
    • Downstream Rab2 effectors unidentified
    • Cargo transiting the Rab2-dependent step not defined
  3. 2024 Medium

    It was unclear whether TgTBC9 acts solely on Rab2; pull-down analysis showed it also directly binds Rab11A and Rab11B, extending its regulatory role to daughter IMC formation alongside early vesicular transport.

    Evidence Pull-down assay, fluorescence localization, and auxin-inducible degron knockdown in T. gondii

    PMID:38762629

    Open questions at the time
    • Single binding method (pull-down) for the interactions
    • Relative preference among Rab2/Rab11A/Rab11B not quantified
    • GAP catalytic activity toward Rab11A/B not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • The Rab2 effectors, guanine nucleotide-exchange factor, membrane cargo, and the biochemical kinetics of TgTBC9-stimulated GTP hydrolysis remain undefined.
  • No Rab2 downstream effector identified
  • No GEF for Rab2 characterized
  • In vitro GAP kinetics not measured

Mechanism profile

Synthesis pass · controlled-vocabulary classification

Evidence

Reading pass · 3 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2024 TgTBC9, a protozoan-specific TBC domain-containing protein localized to the endoplasmic reticulum, acts as a GTPase-activating protein (GAP) for TgRab2; immunoprecipitation and yeast two-hybrid analyses show TgTBC9 preferentially binds Rab2, and the conserved dual-finger active site in the TBC domain is required for GAP function, indicating the TBC9–Rab2 pair controls ER morphology and vesicular trafficking. Immunoprecipitation, yeast two-hybrid, auxin-inducible degron knockdown, active-site mutagenesis (dual-finger motif), fluorescence localization PLoS biology High 38713739
2024 Pull-down assays demonstrate a direct protein–protein interaction between TBC9 and Rab2 (as well as Rab11A and Rab11B), supporting a role for TBC9 in regulating early vesicular transport and daughter inner membrane complex (IMC) formation via these Rab GTPases. Pull-down assay, fluorescence localization, auxin-inducible degron knockdown Communications biology Medium 38762629
2023 TgTBC9 directly binds Rab2 (by immunoprecipitation and yeast two-hybrid) and the TBC9–Rab2 pair controls ER-to-Golgi traffic in T. gondii; knockdown of TgTBC9 disrupts ER and Golgi organization, consistent with loss of Rab2 GAP regulation at this trafficking step. Immunoprecipitation, yeast two-hybrid, auxin-inducible degron knockdown, fluorescence localization bioRxivpreprint Medium 37398139

Source papers

Stage 0 corpus · 3 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2024 Systematic characterization of all Toxoplasma gondii TBC domain-containing proteins identifies an essential regulator of Rab2 in the secretory pathway. PLoS biology 10 38713739
2024 TBC9, an essential TBC-domain protein, regulates early vesicular transport and IMC formation in Toxoplasma gondii. Communications biology 5 38762629
2023 Toxoplasma gondii encodes an array of TBC-domain containing proteins including an essential regulator that targets Rab2 in the secretory pathway. bioRxiv : the preprint server for biology 3 37398139