The Hsp70 chaperone is a major player in stress-induced transposable element activation
The Hsp70 chaperone is a major player in stress-induced transposable element activation
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DOI：
10.1073/pnas.1903936116
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发表时间：
2019-09-03
影响因子：
11.1
通讯作者：
Pimpinelli, Sergio
中科院分区：
文献类型：
--
作者：
Cappucci, Ugo;Noro, Fabrizia;Pimpinelli, Sergio
以往的研究表明，热休克应激可能激活果蝇和其他生物的转座因子（TE）。这种效应取决于分子伴侣复合物的破坏，该分子伴侣复合物通常参与Piwi相互作用RNA（piRNA）的生物发生，Piwi相互作用RNA（piRNA）是涉及TE的表观遗传沉默的最大类别的种系富集的小非编码RNA。然而，一个令人满意的图片如何伴侣可能参与抑制生殖细胞中的TE仍然是未知的。在这里，我们表明，在果蝇中，热休克应激通过诱导型分子伴侣Hsp 70的作用影响皮尔纳生物合成，从而在转录后水平上增加TE的表达。我们发现，应激诱导的TE激活是由Hsp 70与Hsc 70-Hsp 90复合物和其他因子的相互作用触发的，这些因子都参与卵巢和睾丸中的皮尔纳生物合成。这种相互作用诱导所有这些因子向溶酶体的置换，导致皮尔纳生物合成的功能崩溃。这种机制具有明显的进化含义。在剧烈的环境变化中，Hsp 70在增加个体的生存概率和生殖细胞的遗传变异性方面起着关键的双重作用。种群中遗传变异的增加增强了进化的可塑性和可进化性。
Previous studies have shown that heat shock stress may activate transposable elements (TEs) in Drosophila and other organisms. Such an effect depends on the disruption of a chaperone complex that is normally involved in biogenesis of Piwi-interacting RNAs (piRNAs), the largest class of germline-enriched small noncoding RNAs implicated in the epigenetic silencing of TEs. However, a satisfying picture of how chaperones could be involved in repressing TEs in germ cells is still unknown. Here we show that, in Drosophila, heat shock stress increases the expression of TEs at a posttranscriptional level by affecting piRNA biogenesis through the action of the inducible chaperone Hsp70. We found that stress-induced TE activation is triggered by an interaction of Hsp70 with the Hsc70-Hsp90 complex and other factors all involved in piRNA biogenesis in both ovaries and testes. Such interaction induces a displacement of all such factors to the lysosomes, resulting in a functional collapse of piRNA biogenesis. This mechanism has clear evolutionary implications. In the presence of drastic environmental changes, Hsp70 plays a key dual role in increasing both the survival probability of individuals and the genetic variability in their germ cells. The consequent increase of genetic variation in a population potentiates evolutionary plasticity and evolvability.