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首页> 外文期刊>BMC Neuroscience >Normal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep
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Normal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep

机译：正常的睡眠发作对于秀丽隐杆线虫的生存不是必需的，而FoxO对于睡眠中的代偿性变化很重要

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Sleep deprivation impairs learning, causes stress, and can lead to death. Notch and JNK-1 pathways impact C. elegans sleep in complex ways; these have been hypothesized to involve compensatory sleep. C. elegans DAF-16, a FoxO transcription factor, is required for homeostatic response to decreased sleep and DAF-16 loss decreases survival after sleep bout deprivation. Here, we investigate connections between these pathways and the requirement for sleep after mechanical stress. Reduced function of Notch ligand LAG-2 or JNK-1 kinase resulted in increased time in sleep bouts during development. These animals were inappropriately easy to arouse using sensory stimulation, but only during sleep bouts. This constellation of defects suggested that poor quality sleep bouts in these animals might activate homeostatic mechanisms, driving compensatory increased sleep bouts. Testing this hypothesis, we found that DAF-16 FoxO function was required for increased sleep bouts in animals with defective lag-2 and jnk-1, as loss of daf-16 reduced sleep bouts back to normal levels. However, loss of daf-16 did not suppress arousal thresholds defects. Where DAF-16 function was required differed; in lag-2 and jnk-1 animals, daf-16 function was required in neurons or muscles, respectively, suggesting that disparate tissues can drive a coordinated response to sleep need. Sleep deprivation due to mechanical stimulation can cause death in many species, including C. elegans, suggesting that sleep is essential. We found that loss of sleep bouts in C. elegans due to genetic manipulation did not impact their survival, even in animals lacking DAF-16 function. However, we found that sleep bout deprivation was often fatal when combined with the concurrent stress of mechanical stimulation. Together, these results in C. elegans confirm that Notch and JNK-1 signaling are required to achieve normal sleep depth, suggest that DAF-16 is required for increased sleep bouts when signaling decreases, and that failure to enter sleep bouts is not sufficient to cause death in C. elegans, unless paired with concurrent mechanical stress. These results suggest that mechanical stress may directly contribute to death observed in previous studies of sleep deprivation and/or that sleep bouts have a uniquely restorative role in C. elegans sleep.
机译：睡眠不足会损害学习，引起压力并可能导致死亡。 Notch和JNK-1途径以复杂的方式影响秀丽隐杆线虫的睡眠。假设这些涉及代偿性睡眠。秀丽隐杆线虫DAF-16（FoxO转录因子）是减少睡眠的稳态反应所必需的，而DAF-16的丧失会降低睡眠发作后的存活率。在这里，我们研究了这些途径与机械应激后睡眠需求之间的联系。 Notch配体LAG-2或JNK-1激酶的功能降低导致发育过程中睡眠发作的时间增加。这些动物在使用感觉刺激时不恰当地容易引起唤醒，但仅在睡眠发作期间。这一系列缺陷表明，这些动物的睡眠质量差可能会激活体内平衡机制，导致代偿性睡眠增加。通过检验该假设，我们发现滞后2和jnk-1有缺陷的动物增加睡眠周期需要DAF-16 FoxO功能，因为daf-16的丧失会使睡眠周期恢复到正常水平。但是，失去daf-16并不能抑制唤醒阈值缺陷。需要DAF-16功能的地方有所不同;在lag-2和jnk-1动物中，神经元或肌肉分别需要daf-16功能，这表明不同的组织可以促进对睡眠需求的协调反应。机械刺激导致的睡眠剥夺可导致包括秀丽隐杆线虫在内的许多物种死亡，这表明睡眠是必不可少的。我们发现，即使在缺乏DAF-16功能的动物中，由于遗传操纵而导致秀丽隐杆线虫失去睡眠也不会影响其存活。但是，我们发现，与机械刺激并发的压力相结合时，睡眠发作剥夺通常是致命的。总的来说，秀丽隐杆线虫的这些结果证实，Notch和JNK-1信号传导是达到正常睡眠深度所必需的;这表明，当信号传导减少时，增加睡眠次数需要DAF-16，并且无法进入睡眠次数不足以导致线虫死亡，除非同时出现机械应力。这些结果表明，机械压力可能直接导致先前在睡眠剥夺研究中观察到的死亡，并且/或者睡眠发作在秀丽隐杆线虫的睡眠中具有独特的恢复作用。

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