Sexual development in Plasmodium Malaria-causing parasites (Plasmodium) have complex life histories in the tissues of humans. For the most part, the parasites focus their efforts on replication within the human host cells. However, occasionally, some replicating cells release gametes into the bloodstream, which are picked up by biting mosquitoes. Filarsky et al. discovered that the Plasmodium parasite keeps the production of gametes under tight epigenetic control using heterochromatin protein 1 (HP1). Plasmodium gametocytogenesis is initiated when HP1 is evicted from upstream of gamete-specific genes by gametocyte development 1 (GDV1) protein. GDV1 is in turn regulated by its antisense RNA. What triggers GDV1 expression remains unclear. Elucidating this pathway could provide a target for interrupting malaria transmission. Science, this issue p. 1259 Plasmodium replication is interrupted for gamete production by eviction of a heterochromatin binding protein upstream of the relevant genes. Malaria is caused by Plasmodium parasites that proliferate in the bloodstream. During each replication cycle, some 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 in proliferating parasites. In this study, we identified Plasmodium falciparum gametocyte development 1 (GDV1) as an upstream activator of sexual commitment. We found that GDV1 targeted heterochromatin and triggered HP1 eviction, thus derepressing ap2-g. Expression of GDV1 was responsive to environmental triggers of sexual conversion and controlled via a gdv1 antisense RNA. Hence, GDV1 appears to act as an effector protein that induces sexual differentiation by antagonizing HP1-dependent gene silencing.

中文翻译：

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GDV1通过拮抗HP1依赖性基因沉默诱导疟疾寄生虫的性承诺

疟原虫引起疟疾的寄生虫（疟原虫）的性发育在人类组织中具有复杂的生活史。在大多数情况下，寄生虫将精力集中在人类宿主细胞内的复制上。然而，偶尔，一些复制细胞会将配子释放到血液中，这些配子会被蚊子叮咬。菲拉斯基等人。发现疟原虫寄生虫使用异染色质蛋白1（HP1）将配子的产生保持在严格的表观遗传控制之下。当 HP1 被配子体发育 1 (GDV1) 蛋白从配子特异性基因的上游驱逐时，疟原虫的配子细胞发生就开始了。GDV1 反过来又受其反义 RNA 的调节。什么触发 GDV1 表达仍不清楚。阐明这一途径可以为阻断疟疾传播提供一个目标。科学，本期第 3 页。1259 通过驱逐相关基因上游的异染色质结合蛋白来中断疟原虫的复制以产生配子。疟疾是由在血液中增殖的疟原虫引起的。在每个复制周期中，一些寄生虫分化成配子体，这是唯一能够感染蚊媒并传播疟疾的形式。性承诺由 AP2-G 的激活触发，AP2-G 是配子细胞发生的主要转录调节因子。异染色质蛋白 1 (HP1) 依赖的 ap2-g 沉默可防止增殖寄生虫的性转化。在这项研究中，我们将恶性疟原虫配子体发育 1 (GDV1) 确定为性承诺的上游激活剂。我们发现 GDV1 靶向异染色质并触发 HP1 驱逐，从而抑制 ap2-g。GDV1 的表达对性转化的环境触发器有反应，并通过 gdv1 反义 RNA 进行控制。因此，GDV1 似乎作为一种效应蛋白，通过拮抗 HP1 依赖性基因沉默来诱导性别分化。