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首页> 外文期刊>Biology Open >Maintenance of muscle myosin levels in adult C. elegans requires both the double bromodomain protein BET-1 and sumoylation
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Maintenance of muscle myosin levels in adult C. elegans requires both the double bromodomain protein BET-1 and sumoylation

机译：维持成年秀丽隐杆线虫的肌肉肌球蛋白水平需要双溴结构域蛋白BET-1和sumoylation

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Attenuation of RAS-mediated signalling is a conserved process essential to control cell proliferation, differentiation, and apoptosis. Cooperative interactions between histone modifications such as acetylation, methylation and sumoylation are crucial for proper attenuation in C. elegans , implying that the proteins recognising these histone modifications could also play an important role in attenuation of RAS-mediated signalling. We sought to systematically identify these proteins and found BET-1. BET-1 is a conserved double bromodomain protein that recognises acetyl-lysines on histone tails and maintains the stable fate of various lineages. Unexpectedly, adults lacking both BET-1 and SUMO-1 are depleted of muscle myosin, an essential component of myofibrils. We also show that this muscle myosin depletion does not occur in all animals at a specific time, but rather that the penetrance of the phenotype increases with age. To gain mechanistic insights into this process, we sought to delay the occurrence of the muscle myosin depletion phenotype and found that it requires caspase activity and MEK-dependent signalling. We also performed transcription profiling on these mutants and found an up-regulation of the FGF receptor, egl-15 , a tyrosine kinase receptor acting upstream of MEK. Consistent with a MEK requirement, we could delay the muscle phenotype by systemic or hypodermal knock down of egl-15 . Thus, this work uncovered a caspase- and MEK-dependent mechanism that acts specifically on ageing adults to maintain the appropriate net level of muscle myosin.
机译：RAS介导的信号传导的减弱是控制细胞增殖，分化和凋亡必不可少的保守过程。组蛋白修饰（例如乙酰化，甲基化和磺酰化）之间的协同相互作用对于秀丽隐杆线虫的适当衰减至关重要，这意味着识别这些组蛋白修饰的蛋白质也可能在RAS介导的信号传导衰减中起重要作用。我们试图系统地鉴定这些蛋白质并发现BET-1。 BET-1是一种保守的双溴结构域蛋白，可识别组蛋白尾巴上的乙酰赖氨酸并维持各种谱系的稳定命运。出乎意料的是，同时缺乏BET-1和SUMO-1的成年人会耗尽肌肌球蛋白，这是肌原纤维的重要组成部分。我们还表明，并非在特定时间在所有动物中都发生肌肉肌球蛋白耗竭，而是随着年龄的增长，表型的渗透率增加。为了获得对该过程的机械见解，我们试图延迟肌肉肌球蛋白消耗表型的发生，并发现它需要胱天蛋白酶活性和MEK依赖性信号传导。我们还对这些突变体进行了转录分析，发现FGF受体egl-15（一种在MEK上游起作用的酪氨酸激酶受体）的上调。与MEK要求一致，我们可以通过egl-15的全身性或皮下性击倒来延迟肌肉表型。因此，这项工作揭示了一种依赖胱天蛋白酶和MEK的机制，该机制专门作用于成年人，以维持适当的肌球蛋白净水平。

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