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首页> 外文期刊>Developmental biology >MGL-1 on AIY neurons translates starvation to reproductive plasticity via neuropeptide signaling in Caenorhabditis elegans
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MGL-1 on AIY neurons translates starvation to reproductive plasticity via neuropeptide signaling in Caenorhabditis elegans

机译:AIY神经元的MGL-1通过Caenorhabditis elegans的神经肽信号传导转化为生殖塑性的饥饿塑性

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Abstract Reproductive plasticity is the ability of an animal to modulate its reproductive functions in response to environmental changes. For example, Caenorhabditis elegans, a free-living nematode, can adjust the onsets of oogenesis and embryogenesis under harsh environmental conditions, including starvation. However, the molecular mechanisms used to perceive and translate environmental signals into reproductive functional adjustments remain largely uncharacterized. We discovered that in C. elegans , the glutamate receptor homolog MGL-1 initiated reproductive plasticity in response to starvation. A genetic analysis of the mutant gene, mgl-1(tm1811) , suggested that starvation delayed the onsets of oogenesis and embryogenesis via MGL-1. Cell-specific rescues of mgl-1 deletion mutants, which used transgenic lines designed to express MGL-1 in different neurons (e.g., RMD, AIA, AIY, and NSM), suggested that only AIY-rescued animals exhibited normal delays in oogenesis and embryogenesis equivalent to those of wild-type animals, suggesting recovery. Furthermore, in AIY neurons, MGL-1 appears to use neuropeptide signaling, rather than glutamate, to translate starvation stimuli into delayed oogenesis and embryogenesis. Our findings, which reveal molecular linkages between starvation signals and reproductive alterations, may provide a basis for understanding energy reallocation mechanisms, as the mgl-1 deletion mutant exhibited more severe reductions in lifespan and fat accumulation than did wild-type animals under starvation conditions. Taken together, MGL-1 is the molecular driver underlying the translation of starvation signals to reproduction plasticity in an AIY neuron-specific manner. Highlights ? MGL-1 delays oogenesis and embryogenesis in response to starvation. ? MGL-1 exerts effects on reproductive plasticity via AIY neurons. ? MMGL-1 use neuropeptides in AIY neurons to adjust reproduction under starvation. ? m gl-1(-) plays a trade-off role between less fat deposit and lifespan under starvation.
机译:摘要繁殖可塑性是动物在响应环境变化时调节其生殖功能的能力。例如,一种自由活性线虫的Caenorhabditise elegans可以在恶劣的环境条件下调整胚芽内发生和胚胎发生的持续性,包括饥饿。然而,用于感知和将环境信号转化为生殖功能调整的分子机制仍然很大程度上是无比的。我们发现,在C.杆状杆菌中,谷氨酸受体同源物MGL-1响应饥饿而启动的生殖塑性。突变基因MGL-1(TM1811)的遗传分析表明,饥饿延迟了通过MGL-1延迟了胚芽和胚胎发生的垂直。 MGL-1缺失突变体的细胞特异性rescup,其使用设计用于表达不同神经元(例如,RMD,AIA,AIY和NSM)表达MGL-1的转基因株系,表明只有AIY-救出的动物才表现出ofoferesis的正常延迟胚胎发生相当于野生型动物的胚胎,表明恢复。此外,在AIY神经元中,MGL-1似乎使用神经肽信号传导而不是谷氨酸,将饥饿刺激转化为延迟的ofoferis和胚胎发生。我们发现饥饿信号和繁殖改变之间的分子键的发现可以为了解能量重新分配机制提供基础,因为MGL-1缺失突变体表现出比饥饿条件下的野生型动物更严重的寿命和脂肪积累。在一起,MGL-1是以AIY神经元特异性方式转换为饥饿信号的分子驱动器。强调 ? MGL-1延迟OutOcesis和胚胎发生响应饥饿。还是MGL-1通过AIY神经元对生殖塑性的影响施加影响。还是MMGL-1使用AIY神经元中的神经肽在饥饿下调整繁殖。还是M GL-1( - )在饥饿下的脂肪存款和寿命较少之间发挥权衡作用。

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