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通过 Pkc53E 介导的磷酸化抑制 Notch 信号转导子 CSL，抵御 寄生虫免疫挑战。

Inhibition of the Notch signal transducer CSL by Pkc53E-mediated phosphorylation to fend off parasitic immune challenge in .

机构信息

Department of Molecular Genetics, Institute of Biology, University of Hohenheim, Stuttgart, Germany.

Department of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany.

出版信息

Elife. 2024 Nov 6;12:RP89582. doi: 10.7554/eLife.89582.

DOI:10.7554/eLife.89582
PMID:39503739
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11540305/
Abstract

Notch signalling activity regulates hematopoiesis in and vertebrates alike. Parasitoid wasp infestation of larvae, however, requires a timely downregulation of Notch activity to allow the formation of encapsulation-active blood cells. Here, we show that the CSL transcription factor Suppressor of Hairless [Su(H)] is phosphorylated at Serine 269 in response to parasitoid wasp infestation. As this phosphorylation interferes with the DNA binding of Su(H), it reversibly precludes its activity. Accordingly, phospho-deficient mutants are immune-compromised. A screen for kinases involved in Su(H) phosphorylation identified Pkc53E, required for normal hematopoiesis as well as for parasitoid immune response. Genetic and molecular interactions support the specificity of the Su(H)-Pkc53E relationship. Moreover, phorbol ester treatment inhibits Su(H) activity in vivo and in human cell culture. We conclude that Pkc53E targets Su(H) during parasitic wasp infestation, thereby remodelling the blood cell population required for wasp egg encapsulation.

摘要

Notch 信号通路活性在无脊椎动物和脊椎动物中都调节着造血过程。然而，寄生蜂对 幼虫的侵袭需要 Notch 活性的及时下调，以允许形成具有包被活性的血细胞。在这里，我们表明， CSL 转录因子 Suppressor of Hairless [Su(H)]在受到寄生蜂侵袭时会在丝氨酸 269 处发生磷酸化。由于这种磷酸化干扰了 Su(H)的 DNA 结合，因此可逆地阻止了其活性。因此，磷酸化缺陷的 突变体免疫功能受损。一个针对参与 Su(H)磷酸化的激酶的筛选发现了 Pkc53E，它不仅对正常造血，而且对寄生蜂免疫反应都是必需的。遗传和分子相互作用支持 Su(H)-Pkc53E 关系的特异性。此外，佛波酯处理在体内和人细胞培养中抑制 Su(H)的活性。我们得出结论，Pkc53E 在寄生蜂侵袭期间靶向 Su(H)，从而重塑了为蜂卵包被所需的血细胞群体。

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