Gujar Hemant, Palli Subba Reddy
Department of Entomology, University of Kentucky, Lexington, KY 40546-0091, USA.
Sci Rep. 2016 May 17;6:26092. doi: 10.1038/srep26092.
The common bed bug is an obligate hematophagous parasite of humans. We studied the regulation of molting and metamorphosis in bed bugs with a goal to identify key players involved. qRT-PCR studies on the expression of genes known to be involved in molting and metamorphosis showed high levels of Krüppel homolog 1 [Kr-h1, a transcription factor that plays key roles in juvenile hormone (JH) action] mRNA in the penultimate nymphal stage (N4). However, low levels of Kr-h1 mRNA were detected in the fifth and last nymphal stage (N5). Knockdown of Kr-h1 in N4 resulted in a precocious development of adult structures. Kr-h1 maintains the immature stage by suppressing E93 (early ecdysone response gene) in N4. E93 expression increases during the N5 in the absence of Kr-h1 and promotes the development of adult structures. Knockdown of E93 in N5 results in the formation of supernumerary nymphs. The role of JH in the suppression of adult structures through interaction with Kr-h1 and E93 was also studied by the topical application of JH analog, methoprene, to N5. Methoprene induced Kr-h1 and suppressed E93 and induced formation of the supernumerary nymph. These data show interactions between Kr-h1, E93 and JH in the regulation of metamorphosis in the bed bugs.
普通臭虫是人类专性吸血寄生虫。我们研究了臭虫蜕皮和变态的调控，目的是确定其中涉及的关键因子。对已知参与蜕皮和变态的基因表达进行的qRT-PCR研究表明，在倒数第二若虫期（N4），克氏同源蛋白1（Kr-h1，一种在保幼激素（JH）作用中起关键作用的转录因子）的mRNA水平很高。然而，在第五龄也是最后一龄若虫期（N5）检测到的Kr-h1 mRNA水平较低。在N4期敲低Kr-h1会导致成虫结构早熟发育。Kr-h1通过在N4期抑制E93（早期蜕皮激素反应基因）来维持未成熟阶段。在没有Kr-h1的情况下，E93在N5期表达增加，并促进成虫结构的发育。在N5期敲低E93会导致多生若虫的形成。我们还通过向N5期臭虫局部施用JH类似物烯虫酯，研究了JH通过与Kr-h1和E93相互作用在抑制成虫结构方面的作用。烯虫酯诱导Kr-h1表达，抑制E93表达，并诱导多生若虫的形成。这些数据表明，Kr-h1、E93和JH在臭虫变态调控中存在相互作用。
