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首页> 外文期刊>The Journal of Experimental Biology >Stress signaling: coregulation of hemoglobin and male sex determination through a terpenoid signaling pathway in a crustacean
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Stress signaling: coregulation of hemoglobin and male sex determination through a terpenoid signaling pathway in a crustacean

机译：应激信号传导：甲壳类动物中萜类信号传导途径对血红蛋白的调节和男性性别决定

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摘要

Environmental signals can activate neuro-endocrine cascades that regulate various physiological processes. In the present study, we demonstrate that two responses to environmental stress signaling in the crustacean Daphnia magna - hemoglobin accumulation and male offspring production - are co-elevated by the crustacean terpenoid hormone methyl farnesoate and several synthetic analogs. Potency of the hormones with respect to the induction of both hemoglobin and male offspring was highly correlated, suggesting that both processes are regulated by the same terpenoid signaling pathway. Six clones of the D. pulex/pulicaria species complex that were previously characterized as unable to produce male offspring and five clones that were capable of producing males were evaluated for both hemoglobin induction and male offspring production in response to methyl farnesoate. Four of the five male-producing clones produced both hemoglobin and male offspring in response to the hormone. Five of the six non-male-producing clones produced neither hemoglobin nor males in response to the hormone. These results provide additional evidence that both physiological processes are regulated by the same signaling pathway. Furthermore, the results indicate that the non-male-producing clones are largely defective in some methyl farnesoate signaling component, downstream from methyl farnesoate synthesis but upstream from the genes regulated by the hormone. A likely candidate for the site of the defect is the methyl farnesoate receptor. As a consequence of this defect, non-male-producing clones have lost their responsiveness to environmental signals that are transduced by this endocrine pathway. This defect in signaling would be likely to enhance population growth in stable environments due to the elimination of males from the population, assuming that other processes critical to population growth are not also compromised by this defect.
机译：环境信号可以激活调节各种生理过程的神经内分泌级联反应。在本研究中，我们证明了甲壳类萜类激素甲基法呢素和几种合成类似物共同提高了甲壳类水蚤在环境应激信号传导中的两种反应-血红蛋白积累和雄性后代产生。激素对血红蛋白和雄性后代的诱导均高度相关，表明这两个过程均受相同的萜类信号传导途径调控。对先前被表征为不能产生雄性后代的D.pulex / pulicaria物种复合体的六个克隆和能够产生雄性的五个克隆进行了血红蛋白诱导和响应于法呢酸甲酯的雄性后代生产。五个产生雄性的克隆中有四个产生了血红蛋白和雄性后代，以响应激素。六个非雄性产生的克隆中有五个既不产生血红蛋白也不产生雄性激素。这些结果提供了另外的证据，即两个生理过程都受同一信号通路调控。此外，结果表明，非雄性产生的克隆在法呢酸甲酯合成下游但在激素调节的基因上游的某些法呢酸甲酯信号组件中存在很大缺陷。缺陷部位的可能候选物是法尼酸甲酯受体。由于该缺陷的结果，非雄性克隆失去了对这种内分泌途径转导的环境信号的响应能力。假设没有其他影响种群增长的过程也不受该缺陷的影响，则这种信号缺陷可能会由于在种群中消除了雄性而在稳定的环境中促进种群增长。

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