repressed mRNAs. In addition, by microarray analysis, Mair et al. found that the expression of 370 other transcripts was also reduced in the DOZI-null mutant. Surprisingly, a large number of transcripts were also increased in abundance in the DOZI-null mutant. As the authors point out, these results suggest that the putative RNA helicase plays a critical role in maintaining steady-state levels of gametocyte-specific transcripts. This work further substantiates the phenomenon of translational repression in Plasmodium and its importance in regulating sexual development of these parasites. Given the widespread occurrence of translational repression and its role in both temporal and spatial gene expression, this should perhaps not be so surprising. The finding raises a number of provocative questions, however. How do translationally silent mRNPs undergo assembly-disassembly cycles? What triggers this process in the insect gut? When released from mRNPs, how do the once-silent mRNAs move from the cytoplasmic mRNPs to cytoplasmic polysomes for expression? The discovery that hundreds of mRNAs are influenced by the mutation of DOZI suggests that the putative helicase plays a pivotal role in control of sexual development in these important parasites. It may also be that closely related parasites, such as Toxoplasma, use a similar mechanism. The recent completion of several protozoan parasite genomes reveals a surprising lack of canonical transcription factors indicating that post-transcriptional
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Burton et al. (2006) studied this question.
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