Rana Zaheer A, Gundersen Kristian, Buonanno Andres, Vullhorst Detlef
Section of Molecular Neurobiology, National Institute of Child Health & Development/NIH, Bethesda, MD, USA.
J Physiol. 2005 Feb 1;562(Pt 3):815-28. doi: 10.1113/jphysiol.2004.075333. Epub 2004 Nov 4.
Firing patterns typical of slow motor units activate genes for slow isoforms of contractile proteins, but it remains unclear if there is a distinct pathway for fast isoforms or if their expression simply occurs in the absence of slow activity. Here we first show that denervation in adult soleus and EDL muscles reverses the postnatal increase in expression of troponin I (TnI) isoforms, suggesting that high-level transcription of both genes in mature muscles is under neural control. We then use a combination of in vivo transfection, live muscle imaging and fluorescence quantification to investigate the role of patterned electrical activity in the transcriptional control of troponin I slow (TnIs) and fast (TnIf) regulatory sequences by directly stimulating denervated muscles with pattern that mimic fast and slow motor units. Rat soleus muscles were electroporated with green fluorescent protein (GFP) reporter constructs harbouring 2.7 and 2.1 kb of TnIs and TnIf regulatory sequences, respectively. One week later, electrodes were implanted and muscles stimulated for 12 days. The change in GFP fluorescence of individual muscle fibres before and after the stimulation was used as a measure for transcriptional responses to different patterns of action potentials. Our results indicate that the response of TnI promoter sequences to electrical stimulation is consistent with the regulation of the endogenous genes. The TnIf and TnIs enhancers were activated by matching fast and slow activity patterns, respectively. Removal of nerve-evoked activity by denervation, or stimulation with a mismatching pattern reduced transcriptional activity of both enhancers. These results strongly suggest that distinct signalling pathways couple both fast and slow patterns of activity to enhancers that regulate transcription from the fast and slow troponin I isoforms.
典型的慢肌运动单位放电模式会激活收缩蛋白慢亚型的基因,但目前尚不清楚是否存在针对快亚型的独特途径,或者它们的表达是否仅在缺乏慢活动的情况下发生。在这里,我们首先表明,成年比目鱼肌和趾长伸肌去神经支配会逆转肌钙蛋白I(TnI)亚型出生后表达的增加,这表明成熟肌肉中这两个基因的高水平转录受神经控制。然后,我们结合体内转染、活体肌肉成像和荧光定量技术,通过用模拟快、慢运动单位的模式直接刺激去神经支配的肌肉,来研究模式化电活动在肌钙蛋白I慢型(TnIs)和快型(TnIf)调控序列转录控制中的作用。分别用携带2.7 kb和2.1 kb TnIs和TnIf调控序列的绿色荧光蛋白(GFP)报告构建体对大鼠比目鱼肌进行电穿孔。一周后,植入电极并对肌肉进行12天的刺激。将刺激前后单个肌纤维的GFP荧光变化用作对不同动作电位模式转录反应的指标。我们的结果表明,TnI启动子序列对电刺激的反应与内源性基因的调控一致。TnIf和TnIs增强子分别通过匹配快、慢活动模式而被激活。去神经支配消除神经诱发的活动,或用不匹配的模式刺激会降低两个增强子的转录活性。这些结果强烈表明,不同的信号通路将快、慢活动模式与调控快、慢肌钙蛋白I亚型转录的增强子联系起来。