BMC Genomics 2006, 7:282 http://www.biomedcentral.com/1471-2164/7/282 dynamics e.g. telomerase [2]. Consequently, MGEs and their derivatives have been identified in almost all organ- isms. Laboratory evidence has repeatedly demonstrated that MGEs can have either a beneficial [3] or detrimental [4] effect on the host's fitness depending on the down- stream effects of transposition. To counteract the detri- mental effects, some organisms have developed protective mechanisms against invading MGEs, such as the repeat- induced point (RIP) mutation system in Neurospora crassa, which silences repetitive elements by methylation and subsequent mutation of cytidine to thymidine nucle- otides [5]. This explains the unusual situation in N. crassa where very few, if any, active MGEs have been detected. MGEs are usually classified according to their mechanism of replication and whether they are autonomous (self-rep- licating) or non-autonomous (dependant on related ele- ments for replication or mobility) [1]. The two broad groups are those which are mobile via either a DNA or RNA mechanism (Figure 1). The DNA group makes use of a self-encoded transposase that facilitates excision and integration from one site to another, while the RNA group utilizes an RNA intermediate and represents a more func- tionally and evolutionarily diverse group of elements. MGEs employing an RNA intermediate use reverse tran- scription to re-invade the genome, increasing their copy number along the way. In the RNA group, long terminal repeat (LTR) retrotransposons are evolutionarily related to retroviruses while the non-LTR retrotransposons form a discrete group and transpose via a unique target primed reverse transcription (TPRT) mechanism [6]. An offshoot of the non-LTR retrotransposons is the non-autonomous non-LTR retrotransposon group. These elements lack the enzymatic machinery for self-replication and mobiliza- tion and their survival depends on hijacking the replica- tive machinery of active non-LTR retrotransposons. MGE open reading frames (ORFs) code for the relevant enzymes that are required for replication and transposi- tion (Figure 1). Another intriguing group of mobile elements are the mobile introns. Divided into three groups based on their mechanisms of mobility (for a review of mobile introns see [7]), these are evolutionarily ancient MGEs and are believed to be the progenitors of non-LTR retrotrans- posons and eukaryotic spliceosomes. The group II introns have an extraordinary array of enzyme activity, including reverse transcriptase, maturase, RNase H and endonucle- ase activity as well as functional ribozymes. To date, group II introns have only been found in organellar genomes (chloroplast and mitochondrial) and a few cyanobacteria. Very little is known about the occurrence of MGEs in Plas- modium species and the role they may have played in the evolution of the parasites' genomes. Initial reports after sequencing of the P. falciparum and P. y. yoelii genomes suggested that there may be a complete absence of MGEs in P. falciparum and no comment was made about MGEs in P. y. yoelii [8,9]. There is bioinformatic and laboratory evidence for the presence of a domesticated derivative of a non-LTR retrotransposon, namely telomerase, in P. fal- ciparum and P. y. yoelii [10-12]. The only other evidence we could find in the literature for MGE-derived or related sequences in Plasmodium spp. are the Alu elements (non autonomous non-LTR retrotransposons) located within the antigen coding genes of P. vivax [13] and the TAREs (telomere associated repetitive elements) found within the multigene superfamilies that code for antigen varia- tion e.g.var, rif and stevor in P. falciparum [14]. The func- tion of these repeats is uncertain although it is proposed that they facilitate antigenic change and immune evasion. We report here a comprehensive genome analysis of potential MGEs and their derivatives in P. falciparum, P. y. yoelii and P. vivax. This provides further insight into Plas- modium genome evolution with particular reference to the compositional bias in P. falciparum. Results Potential MGE domains determined from InterPro and Pfam databases Table 1 lists all the P. falciparum and P. y. yoelii entries with MGE domains in InterPro [15] and Pfam [16] databases. Seven P. y. yoelii and four P. falciparum ORFs were identi- fied. The four P. falciparum ORFs include one with similar- ity to a phage integrase, one with similarity to an intron- encoded nuclease and two domesticated derivatives. InterPro (and Pfam) domains that did not yield any hits in the Plasmodium database PlasmoDB [17] were: IPR000477 (PF00078) Reverse transcriptase; IPR001584 (PF0065) Integrase catalytic domain; IPR002156 (PF00075) Ribonuclease H fold; IPR001037 (PF00552) Retroviral integrase C terminal; IPR003308 (PF02022) Integrase N terminal Zn binding domain; IPR002050 (PF00429) ENV polyprotein; IPR004875 (PF03184) Endonuclease CENP-B protein; IPR008906 (PF05699) hAT element; IPR003322 (PF02337) retroviral GAG pro- tein; IPR005162 (PF03732) retrotransposon GAG pro- tein; IPR000442 (PF01348) Group II intron-encoded maturase; IPR002492 (PF01498) DNA-binding part of catalytic domain of Tc3 transposase; IPR008042 (PF05380) Aspartic protease from PAO retrotransposon family; IPR000305 (PF01541) Group I excinuclease; IPR003545 Telomerase reverse transcriptase; IPR001162 Excinuclease; IPR006350 Intron endonuclease group I; IPR008180 (PF00692) DeoxyUTP pyrophosphatase; IPR001995 (PF00077) Peptidase A2A, retrovirus; IPR000721 (PF00607) retroviral nucleocapsid protein gag (p24). 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