Affinage · Toxoplasma gondii

CDPK2A

calcium-dependent protein kinase CDPK2A · UniProt S8F5F3

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

CDPK2A is a calcium-dependent protein kinase that contributes to the Toxoplasma gondii lytic cycle by regulating microneme discharge, gliding motility, and egress from infected host cells (PMID:37610220). Chemical-genetic and conditional-depletion analyses place CDPK2A upstream of CDPK1 within a signaling module governing motility and egress, and the two kinases are partially functionally redundant (PMID:37610220). Beyond this signaling relationship and the associated lytic-cycle phenotypes, no direct substrates, structural determinants, or activation mechanism of CDPK2A have been characterized in the available corpus.

Mechanistic history

Synthesis pass · year-by-year structured walk · 2 steps
  1. 2023 Medium

    Establishing whether CDPK2A has a functional role in the parasite lytic cycle, this work showed it is a calcium-dependent kinase required for efficient microneme discharge, gliding motility, and host-cell egress.

    Evidence Analog-sensitive kinase alleles and conditional protein depletion with microneme discharge, gliding, and egress readouts in Toxoplasma gondii

    PMID:37610220

    Open questions at the time
    • No direct phosphorylation substrates of CDPK2A identified
    • No structural or biochemical characterization of the kinase's calcium-dependent activation
    • Single-lab study
  2. 2023 Medium

    To resolve how CDPK2A relates to the known egress kinase CDPK1, epistasis analysis positioned CDPK2A upstream of CDPK1 in a shared signaling module with partial redundancy between the two.

    Evidence Genetic epistasis using analog-sensitive kinase alleles combined with conditional depletion of CDPK2A and CDPK1 in Toxoplasma gondii

    PMID:37610220

    Open questions at the time
    • Molecular basis of CDPK2A-to-CDPK1 signaling not defined
    • Extent and mechanism of functional redundancy unquantified
    • Whether CDPK2A directly regulates CDPK1 or acts through intermediates is unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • The direct substrates, activation mechanism, and molecular link between CDPK2A and CDPK1 remain undefined.
  • No phosphoproteomic substrate mapping
  • No structural model of CDPK2A
  • Mechanism of upstream regulation of CDPK1 unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification
Partners
CDPK1 (ACTS DOWNSTREAM OF CDPK2A IN A SHARED SIGNALING MODULE, PARTIALLY REDUNDANT)

Evidence

Reading pass · 2 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2023 CDPK2A is a calcium-dependent protein kinase that contributes to Toxoplasma lytic cycle fitness by regulating microneme discharge, gliding motility, and egress from infected host cells, as demonstrated by chemical-genetic (analog-sensitive kinase allele) and conditional-depletion approaches. Chemical-genetic (analog-sensitive kinase alleles) and conditional protein depletion with phenotypic readouts (microneme discharge, gliding motility, egress assays) mBio Medium 37610220
2023 Genetic epistasis analysis revealed that CDPK2A acts upstream of CDPK1 in a signaling module governing motility and egress, with partial functional redundancy between the two kinases. Genetic epistasis using analog-sensitive kinase alleles combined with conditional depletion of CDPK2A and CDPK1 mBio Medium 37610220

Source papers

Stage 0 corpus · 1 paper · ranked by NIH iCite citations
Year Title Journal Citations PMID
2023 CDPK2A and CDPK1 form a signaling module upstream of Toxoplasma motility. mBio 12 37610220