The PTEX component EXP2 is critical for establishing a patent malaria infection in mice Kalanon, Ming, Bargieri, Daniel, Sturm, Angelika, Matthews, Kathryn, Ghosh, Sreejoyee, Goodman, Christopher D., Thiberge, Sabine, Mollard, Vanessa, McFadden, Geoffrey I., Menard, Robert and de Koning-Ward, Tania F. 2016, The PTEX component EXP2 is critical for establishing a patent malaria infection in mice, Cellular microbiology, vol. 18, no. 3, pp. 399-412, doi: 10.1111/cmi.12520. Attached Files Name Description MIMEType Size Downloads Title The PTEX component EXP2 is critical for establishing a patent malaria infection in mice Author(s) Kalanon, Ming Bargieri, Daniel Sturm, Angelika Matthews, Kathryn Ghosh, Sreejoyee Goodman, Christopher D. Thiberge, Sabine Mollard, Vanessa McFadden, Geoffrey I. Menard, Robert de Koning-Ward, Tania F. orcid.org/0000-0001-5810-8063 Journal name Cellular microbiology Volume number 18 Issue number 3 Start page 399 End page 412 Total pages 14 Publisher Wiley Place of publication Weinheim, Germany Publication date 2016-03 ISSN 1462-5822 Keyword(s) EXP2 PTEX Plasmodium erythrocyte liver protein export Summary Export of most malaria proteins into the erythrocyte cytosol requires the Plasmodium Translocon of Exported proteins (PTEX) and a cleavable Plasmodium Export Element (PEXEL). In contrast, the contribution of PTEX in the liver stages and export of liver stage proteins is unknown. Here, using the FLP/FRT conditional mutatagenesis system, we generate transgenic P. berghei parasites deficient in EXP2, the putative pore-forming component of PTEX. Our data reveal that EXP2 is important for parasite growth in the liver and critical for parasite transition to the blood, with parasites impaired in their ability to generate a patent blood-stage infection. Surprisingly, whilst parasites expressing a functional PTEX machinery can efficiently export a PEXEL-bearing GFP reporter into the erythrocyte cytosol during a blood stage infection, this same reporter aggregates in large accumulations within the confines of the parasitophorous vacuole membrane during hepatocyte growth. Notably HSP101, the putative molecular motor of PTEX, could not be detected during the early liver stages of infection, which may explain why direct protein translocation of this soluble PEXEL-bearing reporter or indeed native PEXEL proteins into the hepatocyte cytosol has not been observed. This suggests that PTEX function may not be conserved between the blood and liver stages of malaria infection. This article is protected by copyright. All rights reserved. Language eng DOI 10.1111/cmi.12520 Field of Research 110309 Infectious Diseases Socio Economic Objective 920109 Infectious Diseases HERDC Research category C1 Refereed article in a scholarly journal Copyright notice ©2015, Wiley Free to Read? Yes Persistent URL http://hdl.handle.net/10536/DRO/DU:30078601 Document type: Journal Article Collections: Faculty of Health School of Medicine Open Access Collection Related Links Link Description Link to full-text (open access)   Connect to Elements publication management system Go to link with your DU access privileges   Connect to published version Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au. Versions Version Filter Type Wed, 30 Sep 2015, 16:50:05 EST Thu, 01 Oct 2015, 05:20:14 EST Thu, 01 Oct 2015, 08:35:12 EST Thu, 22 Oct 2015, 11:47:29 EST Fri, 23 Oct 2015, 05:11:36 EST Fri, 23 Oct 2015, 09:03:15 EST Fri, 23 Oct 2015, 09:04:30 EST Wed, 28 Oct 2015, 08:13:14 EST Mon, 18 Jul 2016, 15:45:27 EST Sat, 22 Apr 2017, 02:33:12 EST Fri, 09 Feb 2018, 14:25:20 EST Tue, 24 Dec 2019, 07:35:04 EST Sun, 20 Feb 2022, 12:37:06 EST Filtered Full Citation counts:   Cited 27 times in TR Web of Science Cited 27 times in Scopus Search Google Scholar Access Statistics: 609 Abstract Views, 4 File Downloads  -  Detailed Statistics Created: Thu, 22 Oct 2015, 11:47:29 EST