Department of Molecular Microbiology and Immunology, Johns Hopkins Malaria Research Institute, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Proc Natl Acad Sci U S A. 2013 Apr 30;110(18):E1676-84. doi: 10.1073/pnas.1217712110. Epub 2013 Apr 9.
Gametocytes are essential for Plasmodium transmission, but little is known about the mechanisms that lead to their formation. Using piggyBac transposon-mediated insertional mutagenesis, we screened for parasites that no longer form mature gametocytes, which led to the isolation of 29 clones (insertional gametocyte-deficient mutants) that fail to form mature gametocytes. Additional analysis revealed 16 genes putatively responsible for the loss of gametocytogenesis, none of which has been previously implicated in gametocytogenesis. Transcriptional profiling and detection of an early stage gametocyte antigen determined that a subset of these mutants arrests development at stage I or in early stage II gametocytes, likely representing genes involved in gametocyte maturation. The remaining mutants seem to arrest before formation of stage I gametocytes and may represent genes involved in commitment to the gametocyte lineage.
配子体对于疟原虫的传播至关重要，但对于导致其形成的机制知之甚少。我们使用 piggyBac 转座子介导的插入突变筛选，寻找不再形成成熟配子体的寄生虫，这导致分离出 29 个克隆（插入配子体缺陷突变体），这些克隆无法形成成熟配子体。进一步的分析显示，16 个基因可能导致配子体发生缺陷，其中没有一个基因以前与配子体发生有关。转录谱分析和早期配子体抗原的检测表明，这些突变体中的一部分在 I 期或早期 II 期配子体中发育停滞，可能代表参与配子体成熟的基因。其余的突变体似乎在形成 I 期配子体之前就停滞不前，可能代表参与配子体谱系决定的基因。
