Affinage · Plasmodium

Showing PF3D7_0729000 — SRP9 is a alias.

SRP9

PF3D7_0729000 · signal recognition particle subunit SRP9

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

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PF3D7_0729000 (SRP9) is a subunit of the six-polypeptide P. falciparum signal recognition particle, which assembles with a 303 nt SRP RNA to mediate co-translational protein targeting (PMID:24434517). Within this complex, SRP9 partners with SRP14 and Alu RNA to form the Alu domain, which in P. falciparum adopts a non-canonical open Y-shaped conformation rather than the closed loop-loop pseudoknot of human and prokaryotic counterparts; despite this open geometry, the domain binds cytoplasmic P. falciparum ribosomes with nanomolar affinity, a species-specific recognition not reproduced by human ribosomes (PMID:34017052). In parasites, SRP9-GFP shows nucleo-cytoplasmic distribution, and its nuclear import depends on the importin α/β pathway, since the import inhibitor ivermectin blocks nuclear entry of SRP polypeptides including SRP9 at submicromolar concentrations and kills the parasite (PMID:24434517). Beyond its role in the SRP Alu domain and its shuttling behavior, no further gene-specific mechanistic detail for SRP9 has been characterized in the available corpus.

Mechanistic history

Synthesis pass · year-by-year structured walk · 2 steps
  1. 2014 Medium

    Establishing that SRP9 is a bona fide constituent of the parasite SRP and defining its subcellular trafficking answered whether this subunit functions within the P. falciparum SRP and how it reaches its site of action.

    Evidence Transgenic parasites expressing SRP9-GFP with co-localization microscopy and pharmacological nuclear-import inhibition by ivermectin

    PMID:24434517

    Open questions at the time
    • Does not resolve which cargo or targeting events SRP9 specifically supports
    • Killing by ivermectin is not specific to SRP9 and does not isolate its individual contribution
    • No direct demonstration of SRP9 function in co-translational targeting
  2. 2021 High

    Determining the structure of the SRP9/14-Alu RNA domain resolved whether the parasite Alu domain shares the conserved closed architecture and how it engages ribosomes, revealing a divergent open conformation with species-selective ribosome binding.

    Evidence NMR, SAXS, and cryo-EM structural analysis of the Alu domain with ribosome-binding affinity measurements

    PMID:34017052

    Open questions at the time
    • Does not isolate the individual contribution of SRP9 versus SRP14 to the open conformation or ribosome binding
    • Functional consequence of the open geometry for translation retardation in living parasites not demonstrated
    • Structural basis of the P. falciparum ribosome selectivity not defined at residue level

Open questions

Synthesis pass · forward-looking unresolved questions
  • The specific molecular role of SRP9 within the Alu domain, its individual contribution to ribosome binding and translation retardation, and any function outside the SRP complex remain undefined.
  • No subunit-resolved dissection of SRP9 within the Alu heterodimer
  • No direct evidence linking SRP9 to translation elongation arrest in vivo
  • No characterization of SRP9 function independent of the SRP complex

Mechanism profile

Synthesis pass · controlled-vocabulary classification
Complex memberships
SRP Alu domain (SRP9/14 heterodimer with Alu RNA)Signal recognition particle (six-polypeptide SRP9/SRP14/SRP19/SRP54/SRP68/SRP72 with 303 nt SRP RNA)

Evidence

Reading pass · 2 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 P. falciparum SRP9 is one of six polypeptides (SRP9, SRP14, SRP19, SRP54, SRP68, SRP72) that compose the P. falciparum signal recognition particle together with a 303 nt SRP RNA; transgenic parasites expressing SRP9-GFP chimeric protein showed nucleo-cytoplasmic localization, and ivermectin (an importin α/β-mediated nuclear import inhibitor) blocked nuclear import of PfSRP polypeptides including SRP9 at submicromolar concentrations, killing the parasites. Transgenic parasite lines expressing GFP-chimeric proteins, co-localization fluorescence microscopy, pharmacological inhibition with ivermectin Cell death & disease Medium 24434517
2021 The P. falciparum SRP Alu domain, formed by the SRP9/14 heterodimer and Alu RNA, adopts a non-canonical open Y-shaped conformation (rather than the closed loop-loop pseudoknot seen in human/prokaryotic counterparts), as determined by NMR, SAXS, and cryo-EM; cytoplasmic P. falciparum ribosomes recognize both the open PfAlu domain and closed human Alu domain with nanomolar affinity, whereas human ribosomes do not provide high-affinity binding sites for either Alu domain. NMR, SAXS, cryo-EM structural analysis; ribosome-binding affinity measurements Communications biology High 34017052

Source papers

Stage 0 corpus · 3 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Plasmodium falciparum signal recognition particle components and anti-parasitic effect of ivermectin in blocking nucleo-cytoplasmic shuttling of SRP. Cell death & disease 51 24434517
2007 Unraveling the components of protein translocation pathway in human malaria parasite Plasmodium falciparum. Archives of biochemistry and biophysics 25 17919451
2021 Structural analysis of the SRP Alu domain from Plasmodium falciparum reveals a non-canonical open conformation. Communications biology 8 34017052