Perez-Hedo Meritxell, Rivera-Perez Crisalejandra, Noriega Fernando G
Department of Biological Sciences, Florida International University, Miami, Florida, United States of America.
PLoS One. 2014 Jan 29;9(1):e86183. doi: 10.1371/journal.pone.0086183. eCollection 2014.
The interactions between the insulin signaling pathway (ISP) and juvenile hormone (JH) controlling reproductive trade-offs are well documented in insects. JH and insulin regulate reproductive output in mosquitoes; both hormones are involved in a complex regulatory network, in which they influence each other and in which the mosquito's nutritional status is a crucial determinant of the network's output. Previous studies reported that the insulin-TOR (target of rapamacyn) signaling pathway is involved in the nutritional regulation of JH synthesis in female mosquitoes. The present studies further investigate the regulatory circuitry that controls both JH synthesis and reproductive output in response to nutrient availability.
We used a combination of diet restriction, RNA interference (RNAi) and insulin treatments to modify insulin signaling and study the cross-talk between insulin and JH in response to starvation. JH synthesis was analyzed using a newly developed assay utilizing fluorescent tags.
Our results reveal that starvation decreased JH synthesis via a decrease in insulin signaling in the corpora allata (CA). Paradoxically, starvation-induced up regulation of insulin receptor transcripts and therefore "primed" the gland to respond rapidly to increases in insulin levels. During this response to starvation the synthetic potential of the CA remained unaffected, and the gland rapidly and efficiently responded to insulin stimulation by increasing JH synthesis to rates similar to those of CA from non-starved females.
胰岛素信号通路(ISP)与控制生殖权衡的保幼激素(JH)之间的相互作用在昆虫中已有充分记载。JH和胰岛素调节蚊子的生殖输出;这两种激素都参与一个复杂的调节网络,在这个网络中它们相互影响,而且蚊子的营养状况是该网络输出的关键决定因素。先前的研究报道,胰岛素 - TOR(雷帕霉素靶蛋白)信号通路参与雌性蚊子中JH合成的营养调节。本研究进一步探究了响应营养可利用性而控制JH合成和生殖输出的调节回路。
我们结合饮食限制、RNA干扰(RNAi)和胰岛素处理来改变胰岛素信号,并研究胰岛素和JH在饥饿响应中的相互作用。使用一种新开发的利用荧光标签的检测方法分析JH合成。
我们的结果表明,饥饿通过降低咽侧体(CA)中的胰岛素信号来减少JH合成。矛盾的是,饥饿诱导胰岛素受体转录本上调,因此使腺体“做好准备”以快速响应胰岛素水平的升高。在对饥饿的这种反应过程中,CA的合成潜力不受影响,并且腺体通过将JH合成增加到与未饥饿雌性蚊子的CA相似的速率,对胰岛素刺激做出快速而有效的反应。