Dissecting the roles of FTZ-F1 in larval molting and pupation, and the sublethal effects of methoxyfenozide on Helicoverpa armigera.
Dissecting the roles of FTZ-F1 in larval molting and pupation, and the sublethal effects of methoxyfenozide on Helicoverpa armigera.
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DOI：
10.1002/ps.6146
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发表时间：
2020-10
影响因子：
4.1
通讯作者：
Wanna Zhang;Long Ma;Xiangya Liu;Yingchuan Peng;G. Liang;Haijun Xiao
中科院分区：
文献类型：
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作者：
Wanna Zhang;Long Ma;Xiangya Liu;Yingchuan Peng;G. Liang;Haijun Xiao
背景在全变态昆虫中，主要的发育转变，幼虫蜕皮和化蛹，由20-羟基蜕皮激素（20-hydroxyecdysone，20 E）的脉冲触发并由保幼激素协调。甲氧虫酰肼（MF）是一种蜕皮激素激动剂，是一类新型的昆虫生长调节剂，对鳞翅目害虫有较好的防治效果。Fushi-tarazu因子1（FTZ-F1）是蜕皮激素诱导的转录因子。到目前为止，MF对20 E反应基因的影响仍不清楚，我们推测FTZ-F1参与MF的生长调节作用。结果LC 25和LC 10的MF可使棉铃虫严重蜕皮失败，延长幼虫历期，降低蛹重，降低呼吸频率、化蛹率和羽化率。此外，亚致死剂量的MF抑制蜕皮甾体激素的生成，降低内在的20 E滴度，但表现出诱导作用的20 E反应基因，包括HaFTZ-F1。HaFTZ-F1主要表达于幼虫表皮，在蜕皮前后表达显著上调，并在蛹前期维持较高水平。HaFTZ-F1在4龄幼虫中的敲除严重损害幼虫蜕皮，而在末龄幼虫中的敲除引起异常化蛹。此外，敲除HaFTZ-F1下调了三个关键的蜕皮类固醇生成基因，降低了20 E滴度，并抑制了20 E受体和20 E反应基因的表达。将20 E导入HaFTZ-F1-RNAi幼虫后，部分缓解了20 E诱导的信号级联反应的负面影响。结论亚致死剂量MF对H. HaFTZ-F1通过调节20 E滴度及其信号通路来调控棉铃虫的蜕皮和化蛹。
BACKGROUND In holometabolous insects, the major developmental transitions, larval molting and pupation, are triggered by a pulse of 20-hydroxyecdysone (20E) and coordinated by juvenile hormone. Methoxyfenozide (MF), an ecdysteroid agonist, represents a new class of insect growth regulators and is effective against lepidopteran pests. Fushi-tarazu factor 1 (FTZ-F1) is an ecdysone-inducible transcription factor. To date, the effect of MF on 20E-response genes remains unclear, and we speculate the involvement of FTZ-F1 in MF's growth regulating effect. RESULTS MF at LC25 and LC10 caused severe ecdysis failure in Helicoverpa armigera, extended their larval duration, lowered their pupal weight, and reduced the respiratory rate, pupation rate, and emergence rate. Furthermore, sublethal dose of MF inhibited ecdysteroidogenesis and lowered intrinsic 20E titer, but showed an inductive effect on 20E-response genes including HaFTZ-F1. HaFTZ-F1, predominately expressed in larval epidermis, was markedly up-regulated before or right after larval ecdysis, and maintained high level in prepupal stage. Knockdown of HaFTZ-F1 in 4th-instar larvae severely impaired larval ecdysis, while its knockdown in final-instar larvae caused abnormal pupation. Moreover, knocking down HaFTZ-F1 down-regulated three critical ecdysteroidogenesis genes, lowered 20E titer, and suppressed the expression of 20E receptors and 20E-response genes. The introduction of 20E into HaFTZ-F1-RNAi larvae partly relieved the negative effects on 20E-induced signaling cascade. CONCLUSION Our findings reveal the adverse effects of sublethal doses of MF on the development of H. armigera, elucidate the resulting perturbations on 20E-induced signaling cascade, and propose that HaFTZ-F1 regulates ecdysis and pupation by mediating 20E titer and its signaling pathway.