| 2005 |
RON2 (together with RON4 and RON5) was identified as a rhoptry neck protein that associates with the microneme protein AMA1 at the moving junction during host cell invasion, forming a complex derived from two distinct secretory organelles (micronemes and rhoptry necks). |
Co-immunoprecipitation, mass spectrometry, immunofluorescence localization during invasion |
PLoS pathogens |
High |
16244709
|
| 2009 |
RON2 and AMA1 can interact directly in the absence of other MJ complex members (RON4, RON5, RON8), as shown by metabolic labelling and immunoprecipitation. Additionally, RON2 is targeted to the host cell membrane upon secretion, where RON4/5/8 associate with the cytoplasmic face of the host cell membrane. |
Metabolic labelling, immunoprecipitation, differential permeabilization, antibody loading into host cell |
PLoS pathogens |
High |
19247437
|
| 2009 |
RON8 was identified as an additional member of the RON2/4/5 complex at the moving junction. All RON proteins (RON2, RON4, RON5, RON8) are present at the MJ during invasion and undergo proteolytic maturation during trafficking to the rhoptries. |
Biochemical fractionation, Co-immunoprecipitation, immunofluorescence during invasion |
PLoS pathogens |
High |
19247437
|
| 2011 |
RON2 is inserted as an integral membrane protein in the host cell membrane and directly binds AMA1 through a specific region near its C-terminus. This RON2-AMA1 interaction is critical for invasion by both T. gondii and P. falciparum, demonstrated by invasion inhibition assays using recombinant proteins. |
Interaction assays with native and recombinant proteins, invasion inhibition assays, membrane topology analysis |
PLoS pathogens |
High |
21347343
|
| 2011 |
The C-terminus of TgRON2 contains two short segments (D3 and D4) flanking a hydrophobic stretch that independently associate with the ectodomain of TgAMA1. Pre-incubation with D3 peptide (fused to GST) dramatically reduces invasion but does not prevent injection of rhoptry bulb proteins, demonstrating that the RON2 C-terminus forms the crucial bridge between AMA1 and the rest of the MJ complex. |
Deletion mapping, GST-fusion pulldown, invasion inhibition assay, rhoptry injection assay |
PLoS pathogens |
High |
21347354
|
| 2011 |
Crystal structure of TgAMA1 complexed with a RON2 peptide was determined at 1.95 Å resolution, revealing that RON2 binds the hydrophobic groove of AMA1 through a stepwise assembly mechanism creating extensive buried surface area, enabling resistance to mechanical forces during invasion. |
X-ray crystallography at 1.95 Å resolution |
Science (New York, N.Y.) |
High |
21778402
|
| 2012 |
RON5 plays a key role in organization of the MJ RON complex: conditional knockdown of RON5 causes complete degradation of RON2 and mistargeting of RON4 within the secretory pathway, demonstrating that RON5 is required for RON2 stability. Loss of RON5 also abolishes host cell invasion and prevents evacuole formation, but does not impact egress. |
Conditional knockdown (tetracycline-regulatable), immunofluorescence, invasion assay, evacuole assay, egress assay |
PLoS pathogens |
High |
24651769
|
| 2014 |
AMA1 interacts with RON2 to maintain MJ structural integrity in T. gondii and is required for parasite internalization. Disruption of the AMA1 gene results in upregulation of AMA1 and RON2 homologues (paralogues) that cooperate to support residual invasion, demonstrating plasticity in MJ composition. |
Reverse genetics (gene disruption), conditional complementation, invasion assays, immunofluorescence |
Nature communications |
High |
24934579
|
| 2014 |
When Toxoplasma lacks toxofilin and cannot locally remodel cortical actin, the RON2-containing moving junction fails to anchor to the host cell cortex and travels retrogradely, demonstrating that junction anchoring requires host cortex remodeling for efficient invasion. RON2 molecules are eventually posteriorly capped and cleaved/released in failed invasion events. |
Live imaging of fluorescently-tagged RON2, kinematic analysis of >1000 invasion events, toxofilin mutant parasites |
BMC biology |
Medium |
25551479
|
| 2015 |
The AMA1 DII loop governs ligand binding selectivity for RON2; removing the mobile portion of the DII loop (TgAMA1ΔDIIloop) dramatically increases binding affinity for non-cognate RON2 peptides (e.g., EtRON2). Crystal structure of TgAMA1ΔDIIloop with EtRON2 identified spatially distinct anchor points in the AMA1 groove, supporting a model where the DII loop acts as a structural gatekeeper. |
Site-directed mutagenesis, isothermal titration calorimetry, X-ray crystallography |
PloS one |
High |
25955165
|
| 2015 |
TgAMA4 (a sporozoite-expressed AMA paralogue) forms a high-affinity functional complex with its coevolved partner TgRON2L1. Crystal structures of TgAMA4 in apo and TgRON2L1-bound forms revealed an unexpected architecture lacking both a deep surface groove and a key surface loop present in AMA1-RON2 complexes, defining a distinct assembly mechanism. |
Co-crystallization, X-ray crystallography (apo and bound forms), alanine scanning mutagenesis, binding affinity measurements |
Proceedings of the National Academy of Sciences of the United States of America |
High |
26712012
|
| 2016 |
Binding of TgRON2 domain 3 (D3) peptide to TgAMA1 protects AMA1 from rhomboid protease-mediated cleavage of its transmembrane domain, stabilizing AMA1 at the moving junction. Parasites expressing a hypercleavable AMA1 invade less efficiently. Additionally, TgAMA1-TgRON2 interaction leads to dephosphorylation of S527 on the AMA1 cytoplasmic tail, and a phosphomimetic S527D allele causes invasion defects, revealing outside-in signaling through the MJ. |
Peptide treatment assays, cleavage assays, phosphomimetic/phosphoablative AMA1 mutants, invasion efficiency assays |
mBio |
High |
27624124
|
| 2017 |
RON2, RON4, and RON5 cooperate to actively recruit host cell proteins CIN85, CD2AP, and ESCRT-I components ALIX and TSG101 to the moving junction during invasion. Parasite mutants unable to recruit these host proteins show inefficient invasion in culture and attenuated virulence in mice, demonstrating that the RON complex subverts conserved host machinery. |
Co-immunoprecipitation, interaction mapping, parasite mutagenesis, invasion assays, mouse virulence model |
Nature microbiology |
High |
28848228
|
| 2013 |
Sporozoites express paralogue sporoRON2 (RON2L2) that localizes to the apical region and interacts specifically and exclusively with sporoAMA1 (not with generic AMA1), while generic RON2 interacts only with generic AMA1. Pretreatment with domain 3 of sporoRON2 inhibits sporozoite but not tachyzoite invasion, and vice versa for generic RON2 D3, demonstrating stage-specific AMA-RON pairings. |
Co-immunoprecipitation, structural studies of interacting domains, invasion inhibition assays with stage-specific parasites |
PloS one |
High |
23940612
|
| 2023 |
Bradyzoites invade host cells in an MJ-dependent fashion but use paralogue proteins AMA2 and AMA4 (with AMA4 partnering RON2L1) rather than canonical AMA1-RON2. AMA1-RON2 complex immunization induces strong protection against both acute and chronic infection, while AMA4-RON2L1 more selectively targets chronic infection. |
Reverse genetics (gene knockout), invasion assays, immunization/challenge experiments in mice |
Proceedings of the National Academy of Sciences of the United States of America |
High |
36693095
|
| 2017 |
RON4L1 is an additional member of the MJ complex that is targeted to the cytosolic face of the host membrane upon secretion. Critically, RON4L1 trafficking to the MJ is not affected by the absence of RON2, RON4, and RON5, suggesting the co-existence of independent MJ complexes in tachyzoites. |
Immunofluorescence, gene knockout (RON4L1 KO), invasion and virulence assays, triple RON2/4/5-independent localization experiments |
Scientific reports |
Medium |
29263399
|
| 2024 |
RON2-depleted parasites generate a transient host cell membrane conductance increase (invasion pore) prior to invasion but fail to invade, demonstrating that RON2 is not essential for generation of the conductance pathway/pore but is required for productive invasion. Without RON2, the quantal conductance mean differs significantly (0.19 nS vs 0.26 nS for wild-type), implicating RON2 in modulating pore characteristics. |
Electrophysiological recordings at sub-200 µs resolution, RON2-depleted parasites, time-series quantal conductance analysis |
bioRxiv (preprint) / EMBO reports |
Medium |
39416144 40973829
|
| 2024 |
The transcription factor TgAP2XII-9 directly targets RON2 (along with RON4 and RON8) gene loci as shown by CUT&Tag, and its deficiency leads to significant downregulation of rhoptry neck proteins including RON2, resulting in invasion and egress defects, establishing RON2 as a transcriptional target of AP2XII-9 during S/M phase. |
CUT&Tag chromatin profiling, conditional knockdown, invasion and egress assays |
mBio |
Medium |
39207100
|