Department of Microbiology, Immunology, and Molecular Genetics, Long School of Medicine, University of Texas Health Science Center, San Antonio, TX, USA.
Department of Molecular Microbiology and Immunology and South Texas Center for Emerging Infectious Diseases, University of Texas San Antonio, San Antonio, TX, USA.
Epigenetics Chromatin. 2023 Jun 15;16(1):25. doi: 10.1186/s13072-023-00500-y.
Gene expression in malaria parasites is subject to various layers of regulation, including histone post-translational modifications (PTMs). Gene regulatory mechanisms have been extensively studied during the main developmental stages of Plasmodium parasites inside erythrocytes, from the ring stage following invasion to the schizont stage leading up to egress. However, gene regulation in merozoites that mediate the transition from one host cell to the next is an understudied area of parasite biology. Here, we sought to characterize gene expression and the corresponding histone PTM landscape during this stage of the parasite lifecycle through RNA-seq and ChIP-seq on P. falciparum blood stage schizonts, merozoites, and rings, as well as P. berghei liver stage merozoites. In both hepatic and erythrocytic merozoites, we identified a subset of genes with a unique histone PTM profile characterized by a region of H3K4me3 depletion in their promoter. These genes were upregulated in hepatic and erythrocytic merozoites and rings, had roles in protein export, translation, and host cell remodeling, and shared a DNA motif. These results indicate that similar regulatory mechanisms may underlie merozoite formation in the liver and blood stages. We also observed that H3K4me2 was deposited in gene bodies of gene families encoding variant surface antigens in erythrocytic merozoites, which may facilitate switching of gene expression between different members of these families. Finally, H3K18me and H2K27me were uncoupled from gene expression and were enriched around the centromeres in erythrocytic schizonts and merozoites, suggesting potential roles in the maintenance of chromosomal organization during schizogony. Together, our results demonstrate that extensive changes in gene expression and histone landscape occur during the schizont-to-ring transition to facilitate productive erythrocyte infection. The dynamic remodeling of the transcriptional program in hepatic and erythrocytic merozoites makes this stage attractive as a target for novel anti-malarial drugs that may have activity against both the liver and blood stages.
疟原虫的基因表达受到多种调控层的影响,包括组蛋白翻译后修饰(PTMs)。在疟原虫在红细胞内的主要发育阶段,从入侵后的环期到导致逸出的裂殖体期,已经对基因调控机制进行了广泛的研究。然而,介导从一个宿主细胞到下一个宿主细胞的转变的裂殖体的基因调控是寄生虫生物学中一个研究不足的领域。在这里,我们通过对 P. falciparum 血期裂殖体、裂殖体和环期的 Pfalciparum 和 P. berghei 肝期裂殖体进行 RNA-seq 和 ChIP-seq,试图描绘寄生虫生命周期这一阶段的基因表达和相应的组蛋白 PTM 图谱。在肝和红细胞裂殖体中,我们鉴定了一组具有独特组蛋白 PTM 特征的基因,其启动子区域 H3K4me3 耗竭。这些基因在肝和红细胞裂殖体和环期上调,在蛋白质输出、翻译和宿主细胞重塑中发挥作用,并具有共同的 DNA 基序。这些结果表明,类似的调控机制可能是肝和血期裂殖体形成的基础。我们还观察到,在红细胞裂殖体中,H3K4me2 被沉积在编码变体表面抗原的基因家族的基因本体内,这可能有助于这些家族不同成员之间的基因表达切换。最后,H3K18me 和 H2K27me 与基因表达脱耦,并在红细胞裂殖体和裂殖体中富集在着丝粒周围,表明它们在有丝分裂过程中维持染色体组织可能发挥作用。总之,我们的研究结果表明,在裂殖体到环期的过渡期间,基因表达和组蛋白景观发生广泛变化,以促进对红细胞的有效感染。在肝和红细胞裂殖体中,转录程序的动态重塑使其成为新型抗疟药物的有吸引力的靶点,这些药物可能对肝期和血期都有活性。