A Plasmodium Whole-Genome Synteny Map: Indels and Synteny Breakpoints as Foci for Species-Specific Genes
Figure 5
Origin and Putative Mechanism of Expansion of the tstk Family in P. falciparum
(A) Analysis of P. falciparum-specific genes at the SBPs revealed a gene family encoding receptor-associated protein kinases (TSTK). Maximum likelihood distances were calculated for the C-terminal 400 amino acids of all TSTKs, including those found for other Plasmodium species, Toxoplasma gondii, Cryptosporidium parvum, and C. hominis. The tree was rooted using the clade with the three non-Plasmodium sequences as the outgroup (shaded dark gray). The syntenic progenitor genes clearly form one clade (shaded light gray), while the clustering of the other 20 mainly subtelomeric pftstk is more ambiguous (the three non-subtelomeric copies are shown in bold and include pftstk7a, which appears most closely related to the clade of progenitor genes). Circles represent branch points with bootstrap values of 100% (white), 90%–99% (light gray) and 65%–89% (dark gray).
(B) See Figure 2 for the numbering of the SBs and the symbols used in this figure. Based on the 15 recombination events described in Figure 3 and the phylogenetic analysis of the tstk family, we suggest the origin and putative evolution of the pftstk family as shown here. Phylogenetic analysis suggests that the intersyntenic pftstk7a is most closely related to the progenitor founder gene, pftstk0. Interestingly, this gene is the first nonsyntenic gene upstream of SB “VIIe:2b.” This SB is linked in the cRMP genome to SB “I:2a” that in P. falciparum is also flanked by a member of the tstk family, the subtelomeric pftstk1. Based on these observations we suggest that the founder gene pftstk0 was duplicated after the split of P. falciparum from the other Plasmodium species but before SBs “VIIe:2b” and “I:2a” were separated (1). This gene was then directly involved in the breakage of this link, creating Pfchr1 (“I:2a”) and destroying the telomere of “VIId:6d” by addition of “VIIe:2b” (2). During this recombination process, the gene was duplicated and is now present not only as two chromosome-internal copies on “VIIIc:12d” (pftstk0) and between “VIId:6d” and “VIIe:2b” (pftstk7a) but also as a first telomeric copy on the newly formed telomere of Pfchr1 (pftstk1). From here the gene could expand to the other subtelomeric regions (3). Local gene duplications resulted in the generation of seven copies on Pfchr9 and two copies on Pfchr4. After a copy of pftstk ended up at the left-hand cRMP subtelomeric end of SB “Xb:5a,” the telomere conversion linked SB “Xa:12a” to SB “Xb:5a,” which turned this telomeric copy into an intersyntenic gene (pftstk10a). The last non-subtelomeric copy, pftstk13, most likely resulted from a different process of mobility of P. falciparum-specific elements creating the intrasyntenic genes.