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Originally published In Press as doi:10.1074/jbc.M206974200 on September 11, 2002

J. Biol. Chem., Vol. 277, Issue 49, 47524-47532, December 6, 2002
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A Subset of Plasmodium falciparum SERA Genes Are Expressed and Appear to Play an Important Role in the Erythrocytic Cycle*

Susanne K. MillerDagger , Robert T. Good, Damien R. Drew§, Mauro Delorenzi, Paul R. Sanders, Anthony N. Hodder, Terence P. Speed, Alan F. Cowman||, Tania F. de Koning-Ward**, and Brendan S. CrabbDagger Dagger

From the Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia

The Plasmodium falciparum serine repeat antigen (SERA) has shown considerable promise as a blood stage vaccine for the control of malaria. A related protein, SERPH, has also been described in P. falciparum. Whereas their biological role remains unknown, both proteins possess papain-like protease domains that may provide attractive targets for therapeutic intervention. Genomic sequencing has recently shown that SERA and SERPH are the fifth and sixth genes, respectively, in a cluster of eight SERA homologues present on chromosome 2. In this paper, the expression and functional relevance of these eight genes and of a ninth SERA homologue found on chromosome 9 were examined in blood stage parasites. Using reverse transcriptase-PCR and microarray approaches, we demonstrate that whereas mRNA to all nine SERA genes is synthesized late in the erythrocytic cycle, it is those genes in the central region of the chromosome 2 cluster that are substantially up-regulated at this time. Using antibodies specific to each SERA, it was apparent that SERA4 to -6, and possibly also SERA9, are synthesized in blood stage parasites. The reactivity of antibodies from malaria-immune individuals with the SERA recombinant proteins suggested that SERA2 and SERA3 are also expressed at least in some parasite populations. To examine whether SERA genes are essential to blood stage growth, each of the eight chromosome 2 SERA genes was targeted for disruption. Whereas genes at the periphery of the cluster were mostly dispensable (SERA2 and -3 and SERA7 and -8), those in the central region (SERA4 to -6) could not be disrupted. The inability to disrupt SERA4, -5, and -6 is consistent with their apparent dominant expression and implies an important role for these genes in maintenance of the erythrocytic cycle.

* This work was supported by the National Health and Medical Research Council of Australia and by the UNDP/World Bank/WHO Special Program for Research and Training in Tropical Diseases.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Recipient of a Melbourne Research Scholarship (University of Melbourne).

§ Recipient of an NHMRC Peter Doherty postdoctoral award.

Recipient of an Australian Postgraduate Research Award.

|| International Research Scholar of the Howard Hughes Medical Institute.

** Recipient of an NHMRC Howard Florey postdoctoral award.

Dagger Dagger International Research Scholar of the Howard Hughes Medical Institute. To whom all correspondence should be addressed: The Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, VIC 3050, Australia. Tel.: 61-3-9345-2555; Fax: 61-3-9347-0852; E-mail: crabb@wehi.edu.au.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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