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凋亡调节因子的双向控制使DmArgonaute-1对其有更好的掌控。

Two way controls of apoptotic regulators consign DmArgonaute-1 a better clasp on it.

作者信息

Mondal Tanmoy, Bag Indira, Sncvl Pushpavalli, Garikapati Koteswara Rao, Bhadra Utpal, Pal Bhadra Manika

机构信息

Department of Chemical Biology, CSIR-Indian Institute of Chemical Technology, Tarnaka, Hyderabad, Telangana State, India.

Academy of Scientific and Innovative Research (AcSIR), CSIR-IICT Campus, Hyderabad, India.

出版信息

PLoS One. 2018 Jan 31;13(1):e0190548. doi: 10.1371/journal.pone.0190548. eCollection 2018.

DOI:10.1371/journal.pone.0190548
PMID:29385168
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5791970/
Abstract

Argonaute family proteins are well conserved among all organisms. Its role in mitotic cell cycle progression and apoptotic cell elimination is poorly understood. Earlier we have established the contribution of Ago-1 in cell cycle control related to G2/M cyclin in Drosophila. Here we have extended our study in understanding the relationship of Ago-1 in regulating apoptosis during Drosophila development. Apoptosis play a critical role in controlling organ shape and size during development of multi cellular organism. Multifarious regulatory pathways control apoptosis during development among which highly conserved JNK (c-Jun N-terminal kinase) pathway play a crucial role. Here we have over expressed Ago-1 in Drosophila eye and brain by employing UAS (upstream activation sequence)-GAL4 system under the expression of eye and brain specific driver. Over expression of Ago-1 resulted in reduced number of ommatidia in the eye and produced smaller size brain in adult and larval Drosophila. A drastic reversal of the phenotype towards normal was observed upon introduction of a single copy of the dominant negative mutation of basket (bsk, Drosophila homolog of JNK) indicating an active and physical involvement of the bsk with Ago-1 in inducing developmental apoptotic process. Further study showed that Ago-1 stimulates phosphorylation of JNK through transforming growth factor-β activated kinase 1- hemipterous (Tak1-hep) axis of JNK pathway. JNK phosphorylation results in up regulation of pro-apoptotic genes head involution defective (hid), grim & reaper (rpr) and induces activation of Drosophila caspases (cysteinyl aspartate proteinases);DRONC (Death regulator Nedd2-like caspase), ICE (alternatively Drice, Death related ICE-like caspase) and DCP1 (Death caspase-1) by inhibiting apoptotic inhibitor protein DIAP1 (Death-associated inhibitor of apoptosis 1). Further, Ago-1 also inhibits miR-14 expression to trigger apoptosis. Our findings propose that Ago-1 acts as a key regulator in controlling cell death, tumor regression and stress response in metazoan providing a constructive bridge between RNAi machinery and cell death.

摘要

Argonaute家族蛋白在所有生物体中都高度保守。其在有丝分裂细胞周期进程和凋亡细胞清除中的作用尚不清楚。此前我们已经确定了Ago-1在果蝇中与G2/M细胞周期蛋白相关的细胞周期调控中的作用。在此，我们扩展了研究，以了解Ago-1在果蝇发育过程中调节凋亡的关系。凋亡在多细胞生物体发育过程中控制器官形状和大小方面起着关键作用。多种调控途径在发育过程中控制凋亡，其中高度保守的JNK（c-Jun氨基末端激酶）途径起着至关重要的作用。在此，我们通过在眼睛和大脑特异性驱动子的表达下利用UAS（上游激活序列）-GAL4系统在果蝇眼睛和大脑中过表达Ago-1。Ago-1的过表达导致眼睛中小眼数量减少，并在成年和幼虫果蝇中产生较小的大脑。在引入单拷贝的篮状蛋白（bsk，果蝇JNK的同源物）显性负突变后，观察到表型向正常的剧烈逆转，表明bsk与Ago-1在诱导发育性凋亡过程中存在积极的物理相互作用。进一步的研究表明，Ago-1通过JNK途径的转化生长因子-β激活激酶1-半翅目（Tak1-hep）轴刺激JNK的磷酸化。JNK磷酸化导致促凋亡基因头部内卷缺陷（hid）、严峻和收割者（rpr）的上调，并通过抑制凋亡抑制蛋白DIAP1（凋亡相关抑制因子1）诱导果蝇半胱天冬酶（半胱氨酸天冬氨酸蛋白酶）；DRONC（死亡调节因子Nedd2样半胱天冬酶）、ICE（也称为Drice，死亡相关ICE样半胱天冬酶）和DCP1（死亡半胱天冬酶-1）的激活。此外，Ago-1还抑制miR-14的表达以触发凋亡。我们的研究结果表明，Ago-1在控制后生动物的细胞死亡、肿瘤消退和应激反应中起关键调节作用，在RNAi机制和细胞死亡之间提供了一座建设性的桥梁。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc1/5791970/0fa4cbd3f2b5/pone.0190548.g010.jpg
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