GDV1 induces sexual commitment of malaria parasites by antagonizing HP1-dependent gene silencing.
GDV1 induces sexual commitment of malaria parasites by antagonizing HP1-dependent gene silencing.
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DOI：
10.1126/science.aan6042
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发表时间：
2018-03-16
期刊：
影响因子：
--
通讯作者：
Voss TS
中科院分区：
文献类型：
--
作者：
Filarsky M;Fraschka SA;Niederwieser I;Brancucci NMB;Carrington E;Carrió E;Moes S;Jenoe P;Bártfai R;Voss TS
疟疾是由在血液中增殖的疟原虫寄生虫引起的。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子载体并传播疟疾的形式。性承诺是由激活的AP 2-G，主转录调节配子体发生。异染色质蛋白1（HP 1）依赖性沉默ap 2-g防止性转换增殖寄生虫。在这里，我们确定恶性疟原虫配子体发育1（GDV 1）作为性承诺的上游激活剂。我们发现GDV 1靶向异染色质并触发HP 1驱逐，从而解除对ap 2-g的抑制。GDV 1的表达是响应性转换的环境触发和控制通过gdv 1反义RNA。因此，GDV 1似乎作为一种效应蛋白，通过拮抗HP 1依赖的基因沉默诱导性分化。
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. Here, 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 de-repressing 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.
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