CF2 Represses Actin 88F Gene Expression and Maintains Filament Balance during Indirect Flight Muscle Development in Drosophila

CF2 Represses Actin 88F Gene Expression and Maintains Filament Balance during Indirect Flight Muscle Development in Drosophila
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DOI:
10.1371/journal.pone.0010713
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发表时间:
2010-05-25
期刊:
影响因子:
3.7
通讯作者:
Schulz, Robert A.
Schulz, Robert A.
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Gajewski, Kathleen M.;Schulz, Robert A.

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锌指蛋白CF2是果蝇幼虫体壁肌肉中肌肉结构基因的特征性激活剂。为了研究CF2在间接飞行肌(IFM)中的功能,我们检查了携带5个纯合可行突变的果蝇的表型。IFM的总体结构不受影响,但较强的亚型等位基因导致肌原纤维直径增加高达1.5倍。这种尺寸的增加并不引起粗丝和细丝的六聚体排列的任何破坏。RT-PCR分析显示,几个结构基因的转录增加。发育中的IFM中CF 2的异位过表达会破坏肌肉形成。虽然我们的研究结果表明CF 2作为细丝蛋白基因肌动蛋白88 F(Act 88 F)的直接负调节因子的作用,但对肌球蛋白重链(MHC)转录水平的影响似乎是间接的。这种作用与在幼虫肌肉中所描述的直接相反,其中CF2激活结构基因表达。CF 2突变体的肌原纤维表型的变化表明CF 2可能在微调结构基因的表达以确保适当的细丝化学计量以及监测和/或控制最终肌原纤维尺寸方面具有单独的功能。
The zinc finger protein CF2 is a characterized activator of muscle structural genes in the body wall muscles of the Drosophila larva. To investigate the function of CF2 in the indirect flight muscle (IFM), we examined the phenotypes of flies bearing five homozygous viable mutations. The gross structure of the IFM was not affected, but the stronger hypomorphic alleles caused an increase of up to 1.5X in the diameter of the myofibrils. This size increase did not cause any disruption of the hexameric arrangement of thick and thin filaments. RT-PCR analysis revealed an increase in the transcription of several structural genes. Ectopic overexpression of CF2 in the developing IFM disrupts muscle formation. While our results indicate a role for CF2 as a direct negative regulator of the thin filament protein gene Actin 88F (Act88F), effects on levels of transcripts of myosin heavy chain (mhc) appear to be indirect. This role is in direct contrast to that described in the larval muscles, where CF2 activates structural gene expression. The variation in myofibril phenotypes of CF2 mutants suggest the CF2 may have separate functions in fine-tuning expression of structural genes to insure proper filament stoichiometry, and monitoring and/or controlling the final myofibril size.