PDF(Pubmed)
Abstract：
The photoperiodic system is concealed in the highly complex black-box, comprising four functional subunits: 1) a photo/thermo-sensitive input unit, 2) a photoperiodic clock based on a circadian system, 3) a condenser unit counting the number of inductive signals, and 4) a neuroendocrine switch that triggers a phenotypic shift. This review aims to summarize the research history and current reach of our understanding on this subject to connect it with the molecular mechanism of the circadian clock rapidly being unveiled. The review also focuses on the mode of intersubunit information transduction. It will scan the recent advancement in research on each functional subunit, but special attention will be given to the circadian clock-endocrine conjunct and the role of melatonin signaling in the regulation of insect photoperiodism. Prothoracicotropic hormone (PTTH) probably plays the most crucial role in the regulation of pupal diapause, which is the simplest model system of diapause regulation by hormones investigated so far, particularly in the Chinese oak silkmoth (Antheraea pernyi). A search for the trigger to release the PTTH found some candidates, that is, indoleamines. Indolamine metabolism is controlled by arylalkylamine N-acetyltransferase (aaNAT). Indolamine dynamics and aaNAT enzymatic activity changed according to photoperiods. aaNAT activity and melatonin content in the brain showed not only a photoperiodic response but also a circadian fluctuation. aaNAT had multiple E-boxes, suggesting that it is a clock-controlled gene (ccg), which implies that cycle (cyc, or brain-muscle Arnt-like 1 = Bmal1)/Clock (Clk) heterodimer binds to E-box and stimulates the transcription of aaNAT, which causes the synthesis of melatonin. RNAi against transcription modulators, cyc, or Clk downregulated aaNAT transcription, while RNAi against repressor of cyc/Clk, per upregulated aaNAT transcription. Immunohistochemical localization showed that the circadian neurons carry epitopes of melatonin-producing elements such as aaNAT, the precursor serotonin, HIOMT, and melatonin as well as clock gene products such as cyc-ir, Per-ir, and dbt-ir, while PTTH-producing neurons juxtaposed against the clock neurons showed hMT2-ir in A. pernyi brain. Melatonin probably binds to the putative melatonin receptor (MT) that stimulates Ca2+ influx, which in turn activates PKC. This induces Rab 8 phosphorylation and exocytosis of PTTH, leading to termination of diapause. All the PTTH-expressing neurons have PKC-ir, and Rab8-ir. When diapause is induced and maintained under short days, serotonin binding to 5HTR1B suppresses PTTH release in a yet unknown way. RNAi against this receptor knocked out photoperiodism; short day response is blocked and diapause was terminated even under the short day condition. The result showed that a relatively simple system controls both induction and termination in pupal diapause of A. pernyi: the circadian system regulates the transcription of aaNAT as a binary switch, the enzyme produces a melatonin rhythm that gates PTTH release, and 5HTR1B and MT are probably also under photoperiodic regulation. Finally, we listed the remaining riddles which need to be resolved, to fully understand this highly complex system in future studies.
摘要：
光周期系统隐藏在高度复杂的黑匣子中，包括四个功能子单元：1）光敏/热敏输入单元，2)基于昼夜节律系统的光周期时钟，3）一个冷凝器单元计数感应信号的数量，和4)触发表型转变的神经内分泌开关。这篇综述旨在总结我们对这一主题的理解的研究历史和当前范围，以将其与迅速揭晓的昼夜节律时钟的分子机制联系起来。该综述还着重于亚基间信息转导的模式。它将扫描每个功能亚基研究的最新进展，但是将特别注意昼夜节律时钟-内分泌连接以及褪黑激素信号在昆虫光周期调节中的作用。促胸激素(PTTH)可能在调节蛹滞育中起着最关键的作用,这是迄今为止研究的最简单的激素滞育调节模型系统，特别是在中国橡木丝蛾（Antheraeapernyi）中。搜索释放PTTH的触发器找到了一些候选者，也就是说,吲哚胺.吲哚胺代谢受芳基烷基胺N-乙酰转移酶（aaNAT）控制。吲哚胺动力学和aaNAT酶活性随光周期而变化。aaNAT活动和褪黑激素在大脑中的含量不仅显示出光周期反应，而且还显示出昼夜节律波动。aaNAT有多个E-box，这表明它是一个时钟控制的基因（ccg），这意味着这个周期(cyc，或脑肌肉Arnt样1=Bmal1）/Clock（Clk）异二聚体与E盒结合并刺激aaNAT的转录，导致褪黑激素的合成。针对转录调节剂的RNAi，cyc,或者Clk下调aaNAT转录，而针对cyc/Clk阻遏物的RNAi，每个上调的aaNAT转录。免疫组织化学定位显示，昼夜节律神经元携带褪黑激素产生元件如aaNAT的表位，前体血清素，HIOMT,和褪黑激素以及cyc-ir等时钟基因产物，Per-ir,和dbt-ir,而与时钟并列的产生PTTH的神经元在A.pernyi大脑中显示hMT2-ir。褪黑激素可能与假定的褪黑激素受体（MT）结合，刺激Ca2流入，这反过来激活PKC。这诱导Rab8磷酸化和PTTH的胞吐，导致滞育终止。所有表达PTTH的神经元都有PKC-ir，还有Rab8-ir.当诱导滞育并在短时间内维持时，5-羟色胺与5HTR1B结合以未知的方式抑制PTTH释放。针对该受体的RNAi敲除了光周期；即使在短日条件下，短日反应也被阻断，滞育也被终止。结果表明，一个相对简单的系统控制着A.pernyi滞育的诱导和终止：昼夜节律系统作为二进制开关调节aaNAT的转录，这种酶会产生一种褪黑激素的节律来控制PTTH的释放，5HTR1B和MT也可能处于光周期调节下。最后,我们列出了剩下的需要解决的谜语，在未来的研究中充分理解这个高度复杂的系统。
