Mata-Cabana Alejandro, Gómez-Delgado Laura, Romero-Expósito Francisco J, Rodríguez-Palero María J, Artal-Sanz Marta, Olmedo María
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, Seville, Spain.
Andalusian Center for Developmental Biology, Consejo Superior de Investigaciones Científicas - Junta de Andalucía - Department of Molecular Biology and Biochemical Engineering, Universidad Pablo de Olavide, Seville, Spain.
Front Cell Dev Biol. 2020 Nov 10;8:588686. doi: 10.3389/fcell.2020.588686. eCollection 2020.
In a population, chemical communication determines the response of animals to changing environmental conditions, what leads to an enhanced resistance against stressors. In response to starvation, the nematode arrest post-embryonic development at the first larval stage (L1) right after hatching. As arrested L1 larvae, become more resistant to diverse stresses, allowing them to survive for several weeks expecting to encounter more favorable conditions. L1 arrested at high densities display an enhanced resistance to starvation, dependent on soluble compounds released beyond hatching and the first day of arrest. Here, we show that this chemical communication also influences recovery after prolonged periods in L1 arrest. Animals at high density recovered faster than animals at low density. We found that the density effect on survival depends on the final effector of the insulin signaling pathway, the transcription factor DAF-16. Moreover, DAF-16 activation was higher at high density, consistent with a lower expression of the insulin-like peptide DAF-28 in the neurons. The improved recovery of animals after arrest at high density depended on soluble compounds present in the media of arrested L1s. In an effort to find the nature of these compounds, we investigated the disaccharide trehalose as putative signaling molecule, since its production is enhanced during L1 arrest and it is able to activate DAF-16. We detected the presence of trehalose in the medium of arrested L1 larvae at a low concentration. The addition of this concentration of trehalose to animals arrested at low density was enough to rescue DAF-28 production and DAF-16 activation to the levels of animals arrested at high density. However, despite activating DAF-16, trehalose was not capable of reversing survival and recovery phenotypes, suggesting the participation of additional signaling molecules. With all, here we describe a molecular mechanism underlying social communication that allows to maintain arrested L1 larvae ready to quickly recover as soon as they encounter nutrient sources.
在一个种群中，化学通讯决定了动物对不断变化的环境条件的反应，这会增强其对压力源的抵抗力。作为对饥饿的反应，线虫在孵化后于第一幼虫阶段（L1）停止胚胎后发育。作为停止发育的L1幼虫，它们对多种压力的抵抗力增强，使它们能够存活数周，期待遇到更有利的条件。高密度下停止发育的L1幼虫对饥饿的抵抗力增强，这取决于孵化后及停止发育第一天后释放的可溶性化合物。在此，我们表明这种化学通讯也会影响L1长期停止发育后的恢复。高密度的动物比低密度的动物恢复得更快。我们发现密度对生存的影响取决于胰岛素信号通路的最终效应物，即转录因子DAF-16。此外，高密度下DAF-16的激活更高，这与神经元中胰岛素样肽DAF-28的较低表达一致。高密度下停止发育的动物恢复情况的改善取决于停止发育的L1幼虫培养基中存在的可溶性化合物。为了找出这些化合物的性质，我们研究了二糖海藻糖作为假定的信号分子，因为其产量在L1停止发育期间会增加，并且它能够激活DAF-16。我们在停止发育的L1幼虫培养基中检测到低浓度的海藻糖。向低密度下停止发育的动物添加这种浓度的海藻糖足以将DAF-28的产生和DAF-16的激活恢复到高密度下停止发育的动物的水平。然而，尽管海藻糖能激活DAF-16，但它无法逆转生存和恢复表型，这表明还有其他信号分子参与其中。总之，我们在此描述了一种社会通讯背后的分子机制，该机制能使停止发育的L1幼虫保持准备状态，一旦遇到营养源就能迅速恢复。
