Project description:AP2-G is a transcription factor (TF) that is essential for gametocytogenesis of malaria parasites; however, the mechanisms for its inducing the cell linage for sexual reproduction remain unclear. In this paper, this problem is addressed by investigating its expression profile and by determining target genes genome-wide in Plasmodium berghei.
Project description:AP2-G is a transcription factor (TF) that is essential for gametocytogenesis of malaria parasites; however, the mechanisms for its inducing the cell linage for sexual reproduction remain unclear. In this paper, this problem is addressed by investigating its expression profile and by determining target genes genome-wide in Plasmodium berghei.
Project description:AP2-G is a transcription factor (TF) that is essential for gametocytogenesis of malaria parasites; however, the mechanisms for its inducing the cell linage for sexual reproduction remain unclear. In this paper, this problem is addressed by investigating its expression profile and by determining target genes genome-wide in Plasmodium berghei.
Project description:This study elucidates the role of TCF25 as a transcriptional regulator orchestrating sexual conversion in Plasmodium falciparum. Through generation of isogenic tcf25_ko parasite lines, we performed comparative transcriptomic analysis of synchronized ring-stage and schizont-stage parasites (WT vs knockout). Our data demonstrate that tcf25 deletion causes significant dysregulation of both gametocytogenesis-associated genes and antigenic variation gene families. TCF25 directly binds a sexual conversion regulator ap2-g4. These results indicate TCF25 as an essential upstream regulator of malaria parasite sexual development and potential transmission-blocking target.
Project description:This study elucidates the role of TCF25 as a transcriptional regulator orchestrating sexual conversion in Plasmodium falciparum. Through generation of isogenic tcf25_ko parasite lines, we performed comparative transcriptomic analysis of synchronized ring-stage and schizont-stage parasites (WT vs knockout). Our data demonstrate that tcf25 deletion causes significant dysregulation of both gametocytogenesis-associated genes and antigenic variation gene families. TCF25 directly binds a sexual conversion regulator ap2-g4. These results indicate TCF25 as an essential upstream regulator of malaria parasite sexual development and potential transmission-blocking target.
Project description:Commitment to and completion of sexual development are essential for malaria parasites to be transmitted through mosquitoes. The molecular mechanism(s) responsible for these processes however, remain largely unknown. We have identified two transcription factors (both belonging to the AP2 family) essential for gametocytogenesis. AP2-G mutants are characterised by a complete inability to produce gametocytes. In AP2-G2 mutants the gametocytaemia is very significantly reduced but not completely abolished. We have performed the microarray experiments in order to cokmpare the transcriptomes of these mutantnts to the WT parasites and between each other. As P.berghei parasites are characterised by asynchronous development in the rodent host, the different stage composition of the sample would impact the analysis. Therefore parasites were harvested and matured in in vitro to the schizont stage Pairwaise comparison between the mutants and parental line was performed. 3 biological replicates of each condition were used.