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作 者:王菲[1] 李亚明[1] 化晓婷[1] 夏庆友[1]
机构地区:[1]西南大学家蚕基因组生物学国家重点实验室,重庆400716
出 处:《昆虫学报》2012年第9期999-1007,共9页Acta Entomologica Sinica
基 金:重庆市自然科学基金项目(2010BB1017);中央高校基本科研业务费专项(XDJK2009B033)
摘 要:昆虫免疫稳态的维持有赖于准确地激活和有效地抑制Toll或IMD信号通路中的关键转录因子——Dorsal/Dif或Relish。在果蝇等昆虫中,已报道了多种降低转录因子稳定性和活性的免疫稳态调控分子,突变或敲除这类分子导致免疫系统的过度激活。对家蚕Bombyx mori免疫信号通路的研究中,至今为止尚无对这类分子的探索。本研究通过比较基因组学,在家蚕基因组中鉴定了多个可能参与免疫稳态调控的分子,包括Wnt家族成员、Ubc9、FAF和POSH等;并通过检测家蚕被微生物感染后这些分子在多种免疫器官中的诱导表达模式,发现这些分子的表达水平在微生物感染后普遍呈下降趋势,虽然在某些组织中表达量有明显的升高(>1.5倍),但此高表达水平均不能维持且迅速下降;而且免疫稳态调控分子和受其调控的信号通路的对应关系在不同组织中表现出差异。本研究是首次对家蚕免疫稳态调控分子的报道,为深入研究家蚕免疫负调控的分子机制提供了参考。Maintenance of insect immune homeostasis requires prompt activation and down-modulation of the key transcriptional factors : Dorsal/Dif in Toll signaling pathway or Relish in IMD signaling pathway. Several regulatory molecules which modulate the stability or activity of the transcriptional factors in immune response have been identified in Drosophila and some other insects. Mutation or silencing of these molecules leads to over activation of immune system. So far there is no report about the regulatory molecules limiting immune signaling in the silkworm, Bombyx mori. In this study, several molecules which are predicted to be involved in immune homeostasis, including Wnt family members, Ubc9, FAF and POSH, were identified in the silkworm genome by comparative genomic analysis. The expression patterns of these molecules in multiple tissues after microbial infection were recorded, and the results showed that their expression levels generally decreased after microbial infection. Although an increase of more than 1.5-folds in expression level was observed in certain tissues, a rapid decrease followed and the high level was not maintained. Interestingly, the correspondence between the expression patterns of these molecules and the particular signaling pathway that microbes induced varied in different tissues. This is the first report of the regulatory molecules involved in silkworm immune homeostasis, which provides reference for further investigation on the molecular mechanism of immuno-negative modulation in the silkworm.
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