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保幼激素抗性基因耐甲氧普烯控制着赤拟谷盗进入变态发育。

Juvenile hormone resistance gene Methoprene-tolerant controls entry into metamorphosis in the beetle Tribolium castaneum.

作者信息

Konopova Barbora, Jindra Marek

机构信息

Department of Molecular Biology, University of South Bohemia, and Biology Center, Czech Academy of Sciences, 37005 Ceske Budejovice, Czech Republic.

出版信息

Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10488-93. doi: 10.1073/pnas.0703719104. Epub 2007 May 30.

DOI:10.1073/pnas.0703719104
PMID:17537916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1965540/
Abstract

Besides being a spectacular developmental process, metamorphosis is key to insect success. Entry into metamorphosis is controlled by juvenile hormone (JH). In larvae, JH prevents pupal and adult morphogenesis, thus keeping the insect in its immature state. How JH signals to preclude metamorphosis is poorly understood, and a JH receptor remains unknown. One candidate for the JH receptor role is the Methoprene-tolerant (Met) Per-Arnt-Sim (PAS) domain protein [also called Resistance to JH, Rst (1)JH], whose loss confers tolerance to JH and its mimic methoprene in the fruit fly Drosophila melanogaster. However, Met deficiency does not affect the larval-pupal transition, possibly because this process does not require JH absence in Drosophila. By contrast, the red flour beetle Tribolium castaneum is sensitive to developmental regulation by JH, thus making an ideal system to examine the role of Met in the antimetamorphic JH action. Here we show that impaired function of the Met ortholog TcMet renders Tribolium resistant to the effects of ectopic JH and, in a striking contrast to Drosophila, causes early-stage beetle larvae to undergo precocious metamorphosis. This is evident as TcMet-deficient larvae pupate prematurely or develop specific heterochronic phenotypes such as pupal-like cuticular structures, appendages, and compound eyes. Our results demonstrate that TcMet functions in JH response and provide the critical evidence that the putative JH receptor Met mediates the antimetamorphic effect of JH.

摘要

除了是一个壮观的发育过程外,变态是昆虫成功的关键。进入变态受保幼激素(JH)控制。在幼虫中,JH可防止蛹和成虫形态发生,从而使昆虫保持在未成熟状态。目前人们对JH阻止变态的信号传导方式知之甚少,JH受体也仍然未知。JH受体作用的一个候选蛋白是耐甲氧普烯(Met)的Per-Arnt-Sim(PAS)结构域蛋白[也称为对JH的抗性,Rst(1)JH],在果蝇中,其缺失会使果蝇对JH及其类似物甲氧普烯产生耐受性。然而,Met缺失并不影响幼虫到蛹的转变,这可能是因为在果蝇中这个过程并不需要JH的缺失。相比之下,赤拟谷盗对JH的发育调控敏感,因此是研究Met在JH抗变态作用中角色的理想系统。我们在此表明,Met直系同源物TcMet功能受损使拟谷盗对异位JH的作用产生抗性,并且与果蝇形成鲜明对比的是,会导致早期甲虫幼虫过早变态。这表现为TcMet缺陷型幼虫过早化蛹或出现特定的异时表型,如蛹样的表皮结构、附肢和复眼。我们的结果证明TcMet在JH反应中发挥作用,并提供了关键证据,即假定的JH受体Met介导JH的抗变态作用。

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Drosophila melanogaster Methoprene-tolerant (Met) gene homologs from three mosquito species: Members of PAS transcriptional factor family.来自三种蚊虫的黑腹果蝇耐保幼激素(Met)基因同源物:PAS转录因子家族成员。
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