饮食限制和生活史权衡:对鸟类mTOR通路调控和生殖投资的见解

Gebrehaweria Kidane Reda, Sawadi Fransisco Ndunguru, Brigitta Csernus, Gabriella Gulyas, Renata Knop, Csaba Szabo, Levente Czegledi, Adam Z. Lendvai
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摘要

生长、繁殖和生存都需要资源,生物必须在竞争过程中权衡有限的资源。生物体内的营养可用性是通过营养感应途径感知和监测的,这些途径可以触发生理变化或改变基因表达。先前的研究已经提出,当个体在能量预算中遇到限制时,雷帕霉素(mTOR)的机制靶标(mechanistic target of rapamycin)这一信号通路支持一种形式的适应性可塑性。尽管这一过程在进化生物学中具有根本的重要性,但营养限制是如何通过控制这一途径的基因表达来调节的,以及它对适应性的影响仍未得到充分的研究,特别是在鸟类中。本研究以日本鹌鹑为研究对象,采用饮食限制模拟资源耗竭,研究其对日本鹌鹑体重、繁殖和基因表达的影响。鹌鹑分别饲喂20%、30%和40%限制水平的自由采食(ADL) 2周。所有受限制的组都表现出体重减少,而只有在更严格的限制下才观察到鸡蛋数量和质量的减少。饮食限制导致mTOR和胰岛素样生长因子1 (IGF1)表达降低,而核糖体蛋白S6激酶1 (RPS6K1)和自噬相关基因(ATG9A和ATG5)表达上调。mTOR对限制的反应模式与在体重中所看到的相似。无论治疗方式如何,比例较高的生殖投资与mTOR表达的个体差异相关。这些发现揭示了膳食摄入与mTOR及其相关基因表达之间的联系。
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Dietary restriction and life-history trade-offs: insights into mTOR pathway regulation and reproductive investment in birds
Resources are needed for growth, reproduction and survival, and organisms must trade-off limited resources among competing processes. Nutritional availability in organisms is sensed and monitored by nutrient-sensing pathways that can trigger physiological changes or alter gene expression. Previous studies have proposed that one such signalling pathway, the mechanistic target of rapamycin (mTOR), underpins a form of adaptive plasticity when individuals encounter constraints in their energy budget. Despite the fundamental importance of this process in evolutionary biology, how nutritional limitation is regulated through the expression of genes governing this pathway and its consequential effects on fitness remains understudied, particularly in birds. We used dietary restriction to simulate resource depletion and examined its effects on body mass, reproduction and gene expression in Japanese quails (Coturnix japonica). Quails were subjected to ad libitum (ADL) feeding or 20%, 30%, and 40% restriction levels for two weeks. All restricted groups exhibited reduced body mass, whereas reductions in the number and mass of eggs were observed only under more severe restrictions. Dietary restriction led to decreased expression of mTOR and insulin-like growth factor 1 (IGF1), whereas the ribosomal protein S6 kinase 1 (RPS6K1) and autophagy-related genes (ATG9A and ATG5) were upregulated. The pattern in which mTOR respond to restriction was similar to what has been seen in body mass. Regardless of the treatment, proportionally higher reproductive investment was associated with individual variation in mTOR expression. These findings reveal the connection between dietary intake and the expression of mTOR and related genes in this pathway.
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