RON12, a novel Plasmodium-specific rhoptry neck protein important for parasite proliferation
Article first published online: 28 AUG 2013
© 2013 The Authors. Cellular Microbiology published by John Wiley & Sons Ltd.
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How to Cite
Knuepfer, E., Suleyman, O., Dluzewski, A. R., Straschil, U., O'Keeffe, A. H., Ogun, S. A., Green, J. L., Grainger, M., Tewari, R. and Holder, A. A. (2013), RON12, a novel Plasmodium-specific rhoptry neck protein important for parasite proliferation. Cellular Microbiology. doi: 10.1111/cmi.12181
- Article first published online: 28 AUG 2013
- Accepted manuscript online: 12 AUG 2013 08:03AM EST
- Manuscript Accepted: 30 JUL 2013
- Manuscript Revised: 21 JUL 2013
- Manuscript Received: 21 MAR 2013
- UK MRC. Grant Numbers: U117532067, G0900109
- Wellcome Trust Malaria Functional Genomics Initiative. Grant Number: 066742
- US National Institutes of Health. Grant Number: HL078826
- European Union. Grant Numbers: LHSP-CT-2006-036838, 242095
- Wellcome Trust. Grant Number: WT078335MA
Apicomplexan parasites invade host cells by a conserved mechanism: parasite proteins are secreted from apical organelles, anchored in the host cell plasma membrane, and then interact with integral membrane proteins on the zoite surface to form the moving junction (MJ). The junction moves from the anterior to the posterior of the parasite resulting in parasite internalization into the host cell within a parasitophorous vacuole (PV). Conserved as well as coccidia-unique rhoptry neck proteins (RONs) have been described, some of which associate with the MJ. Here we report a novel RON, which we call RON12. RON12 is found only in Plasmodium and is highly conserved across the genus. RON12 lacks a membrane anchor and is a major soluble component of the nascent PV. The bulk of RON12 secretion happens late during invasion (after parasite internalization) allowing accumulation in the fully formed PV with a small proportion of RON12 also apparent occasionally in structures resembling the MJ. RON12, unlike most other RONs is not essential, but deletion of the gene does affect parasite proliferation. The data suggest that although the overall mechanism of invasion by Apicomplexanparasites is conserved, additional components depending on the parasite–host cell combination are required.