Genome plasticity inPlasmodium

Extensive genome plasticity inPlasmodium involves frequent loss of dispensable functions under non-selective conditions, polymorphisms in subtelomeric repetitive regions, as well as rapid and apparently concerted variation in the intra-genic repetitive arrays that are typical of plasmodial antigen genes. As an example of the latter type of variation, the region of the merozoite surface antigen gene MSA-1 ofPlasmodium falciparum, which encodes a tri-peptide repeat, is analysed in detail. The example illustrates how evasion of the immune defenses of the vertebrate host can be achieved through repeat homogenization mechanisms, acting at the DNA level, and leading to rapid fixation of variant epitopes. The remarkable ability of Plasmodia to utilize mechanisms which operate on its own nuclear DNA in the course of mitotic multiplication is discussed against the need of life cycle closure as a haploid unicellular. The possibility is suggested that active genomic diversification in a (clonal) multicellular population evolved as an adaptive tool.