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果蝇跳跃肌肌动蛋白Act79B的缺失通过Act88F的上调得到补偿。

Absence of the Drosophila jump muscle actin Act79B is compensated by up-regulation of Act88F.

作者信息

Dohn Tracy E, Cripps Richard M

机构信息

Department of Biology, University of New Mexico, Albuquerque, New Mexico.

出版信息

Dev Dyn. 2018 Apr;247(4):642-649. doi: 10.1002/dvdy.24616. Epub 2018 Feb 6.

DOI:10.1002/dvdy.24616
PMID:29318731
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6118211/
Abstract

BACKGROUND

Actins are structural components of the cytoskeleton and muscle, and numerous actin isoforms are found in most organisms. However, many actin isoforms are expressed in distinct patterns allowing each actin to have a specialized function. Numerous studies have demonstrated that actin isoforms both can and cannot compensate for each other under specific circumstances. This allows for an ambiguity of whether isoforms are functionally distinct.

RESULTS

In this study, we analyzed mutants of Drosophila Act79B, the predominant actin expressed in the adult jump muscle. Functional and structural analysis of the Act79B mutants found the flies to have normal jumping ability and sarcomere structure. Analysis of actin gene expression determined that expression of Act88F, an actin gene normally expressed in the flight muscles, was significantly up-regulated in the jump muscles of mutants. This indicated that loss of Act79B caused expansion of Act88F expression. When we created double mutants of Act79B and Act88F, this abolished the jump ability of the flies and resulted in severe defects in myofibril formation.

CONCLUSIONS

These results indicate that Act88F can functionally substitute for Act79B in the jump muscle, and that the functional compensation in actin expression in the jump muscles only occurs through Act88F. Developmental Dynamics 247:642-649, 2018. © 2018 Wiley Periodicals, Inc.

摘要

背景

肌动蛋白是细胞骨架和肌肉的结构成分,在大多数生物体中发现了众多肌动蛋白异构体。然而,许多肌动蛋白异构体以不同模式表达,使每种肌动蛋白具有特定功能。众多研究表明,在特定情况下,肌动蛋白异构体既能相互补偿,也不能相互补偿。这使得异构体在功能上是否不同存在模糊性。

结果

在本研究中,我们分析了果蝇Act79B(成体跳跃肌肉中主要表达的肌动蛋白)的突变体。对Act79B突变体的功能和结构分析发现,果蝇具有正常的跳跃能力和肌节结构。对肌动蛋白基因表达的分析确定,Act88F(一种通常在飞行肌肉中表达的肌动蛋白基因)在突变体的跳跃肌肉中的表达显著上调。这表明Act79B的缺失导致Act88F表达的扩展。当我们构建Act79B和Act88F的双突变体时,这消除了果蝇的跳跃能力,并导致肌原纤维形成严重缺陷。

结论

这些结果表明,Act88F在跳跃肌肉中可在功能上替代Act79B,并且跳跃肌肉中肌动蛋白表达的功能补偿仅通过Act88F发生。《发育动力学》247:642 - 649,2018年。©2018威利期刊公司。

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