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Transcriptional regulator HDP1 regulates expansion of the inner membrane complex during early sexual differentiation of malaria parasites [RNA-Seq]

ABSTRACT: Transcriptional regulator HDP1 regulates expansion of the inner membrane complex during early sexual differentiation of malaria parasites [RNA-Seq]

PROVIDER: PRJNA781941 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16983726.fastq.gz	Fastqsanger.gz
	SRR16983727.fastq.gz	Fastqsanger.gz
	SRR16983728.fastq.gz	Fastqsanger.gz

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Transcriptional regulator HDP1 regulates expansion of the inner membrane complex during early sexual differentiation of malaria parasites [RNA-Seq]

Project description:In this study, we identify HDP1, a previously uncharacterized DNA-binding protein first expressed during early sexual differentiation. The development of HDP1-deficient gametocytes arrests at the Stage I to Stage II transition and ends in loss of viability. Analysis of gene expression and HDP1-binding shows that this protein functions as a positive transcriptional regulator of genes essential for gametocyte development, including genes that are critical for the expansion of the inner membrane complex (IMC) that gives P. falciparum gametocytes their characteristic shape.

2021-11-21 | GSE189196 | GEO

Transcriptional regulator HDP1 regulates expansion of the inner membrane complex during early sexual differentiation of malaria parasites [ChIP-Seq]

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Transcriptional regulator HDP1 regulates expansion of the inner membrane complex during early sexual differentiation of malaria parasites

Project description:Transcriptional regulator HDP1 regulates expansion of the inner membrane complex during early sexual differentiation of malaria parasites

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Transcriptional regulator HDP1 regulates expansion of the inner membrane complex during early sexual differentiation of malaria parasites [ChIP-Seq]

Project description:Transcriptional regulator HDP1 regulates expansion of the inner membrane complex during early sexual differentiation of malaria parasites [ChIP-Seq]

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GDV1 triggers sexual conversion and differentiation in malaria parasites by antagonizing HP1-dependent gene silencing

Project description:Malaria is caused by Plasmodium parasites that proliferate through iterative cycles of intra-erythrocytic replication. During each cycle a small number of parasites differentiate into gametocytes, the only forms able to infect the mosquito vector and transmit malaria. Sexual commitment is triggered by activation of AP2-G, the master transcriptional regulator of gametocytogenesis. Heterochromatin protein 1 (HP1)-dependent silencing of ap2-g prevents sexual conversion and secures proliferation. Here, we identify gametocyte development 1 (GDV1) as the first upstream activator of the sexual differentiation pathway in P. falciparum. Induction of GDV1 expression is sufficient to activate AP2-G expression and sexual differentiation. We found that GDV1 targets heterochromatin and triggers HP1 eviction preferentially at ap2-g and other gametocyte-specific genes. We further demonstrate that GDV1-dependent activation of ap2-g is controlled via a gdv1 antisense RNA. In summary, we identify GDV1 as an unprecedented cell fate decision factor that induces sexual differentiation by antagonizing HP1-dependent gene silencing.

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Metabolic competition between lipid metabolism and histone methylation regulates sexual differentiation in human malaria parasites

Project description:Like most pathogens, malaria parasites balance persistence in the current host with transmission to the next. For Plasmodium falciparum, the most widespread and virulent human malaria parasite, persistence depends on continuous asexual replication in red blood cells while transmission requires differentiation into non-replicating gametocytes, the male and female cells able to infect the mosquito vector. This developmental decision is controlled via stochastic derepression of a heterochromatin-silenced locus encoding the transcription factor PfAP2-G, which acts as the master switch for sexual differentiation. Recent work showed that the frequency of pfap2-g derepression is responsive to extracellular levels of phospholipid precursors. However, the regulatory mechanisms linking these metabolites to epigenetic regulation of pfap2-g was hitherto unknown. Using chemical, metabolomic, and genetic approaches, we show that this response is mediated by metabolic competition for the methyl donor S-adenosylmethionine between histone methyltransferases and phospho-ethanolamine methyltransferase, a critical enzyme in the parasite’s pathway for de novo phosphatidyl-choline synthesis. When phosphatidyl-choline precursors are scarce, increased consumption of S-adenosylmethionine for de novo synthesis of phosphatidyl-choline results in a decrease in histone methylation marks that mediate silencing of pfap2-g, thereby up-regulating its transcription and increasing the frequency of sexual differentiation. Our findings reveal a key connection between metabolite utilization and gene expression in malaria parasites that forms the mechanistic link between phosphatidyl-choline metabolism and the frequency of sexual commitment.

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Project description:Single-cell RNA-sequencing is revolutionising our understanding of seemingly homogeneous cell populations but has not yet been widely applied to single-celled organisms. Transcriptional variation in unicellular malaria parasites from the Plasmodium genus is associated with critical phenotypes including red blood cell invasion and immune evasion, yet transcriptional variation at an individual parasite level has not been examined in depth. Here, we describe the adaptation of a single-cell RNA-sequencing (scRNA-seq) protocol to deconvolute transcriptional variation for more than 500 individual parasites of both rodent and human malaria comprising asexual and sexual life-cycle stages. We uncover previously hidden discrete transcriptional signatures during the pathogenic part of the life cycle, suggesting that expression over development is not as continuous as commonly thought. In transmission stages, we find novel, sex-specific roles for differential expression of contingency gene families that are usually associated with immune evasion and pathogenesis.

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Project description:5-methylcytosine (m5C) is emerging as an important epi-transcriptome modification involving RNA stability and translation efficiency in various biological processes. However, it remains unclear how m5C contributes to the dynamic regulation of transcriptome during the development of Plasmodium. Here, we identified the presence of 5-methylcytosine (m5C) modification in rodent (P. yoelii) and human (P. falciparum) malaria parasites transcriptome and depicted a comprehensive characterization landscape of m5C mRNA modification at single-nucleotide resolution (RNA-BisSeq) from asexual replicating stage to gametocyte development. Through transcriptome-wide profiling of mRNA m5C modification, we found that m5C modified mRNA displayed higher stability than non-m5C modified mRNA during the development of Plasmodium. We identified Plasmodium ortholog of NSUN2 as an mRNA m5C methyltransferase in malaria parasites. LC–MS/MS and RNA-BisSeq analysis revealed a large decrease in mRNA m5C modification at transcriptome-wide level upon Nsun2 knockout. Absence of Nsun2 severely reduced gametocyte production in either rodent (P. yoelii) or human (P. falciparum) malaria parasites. Meanwhile, some genes related to gametocytogenesis displayed a great reduction of m5C modification. Together, our data provides comprehensive mRNA m5C profiles in Plasmodium genus and reveals m5C modification-mediated mRNA stability as a novel mechanism regulating sexual differentiation of a unicellular eukaryote.

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5-methylcytosine modification-mediated mRNA stabilization is associated with sexual development of malaria parasites [RNA-seq]

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5-methylcytosine modification-mediated mRNA stabilization is associated with sexual development of malaria parasites [BisRNA-seq]

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