Data from: Vitamin supplementation by gut symbionts ensures metabolic homeostasis in an insect host
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Despite the demonstrated functional importance of gut microbes, our understanding of how animals regulate their metabolism in response to nutritionally beneficial symbionts remains limited. Here, we elucidate the functional importance of the African cotton stainer's (Dysdercus fasciatus) association with two actinobacterial gut symbionts and subsequently examine the insect's transcriptional response following symbiont elimination. In line with bioassays demonstrating the symbionts' contribution towards host fitness through the supplementation of B vitamins, comparative transcriptomic analyses of genes involved in import and processing of B vitamins revealed an upregulation of gene expression in aposymbiotic (symbiont-free) compared with symbiotic individuals; an expression pattern that is indicative of B vitamin deficiency in animals. Normal expression levels of these genes, however, can be restored by either artificial supplementation of B vitamins into the insect's diet or reinfection with the actinobacterial symbionts. Furthermore, the functional characterization of the differentially expressed thiamine transporter 2 through heterologous expression in Xenopus laevis oocytes confirms its role in cellular uptake of vitamin B1. These findings demonstrate that despite an extracellular localization, beneficial gut microbes can be integral to the host's metabolic homeostasis, reminiscent of bacteriome-localized intracellular mutualists.
尽管肠道微生物的功能重要性已得到证实,但我们对动物如何响应营养有益的共生菌以调控自身代谢的认知仍十分有限。本研究阐明了非洲棉红蝽(*Dysdercus fasciatus*)与两种放线菌肠道共生菌的共生关联的功能重要性,并随后探究了共生菌清除后该昆虫的转录响应。与通过补充B族维生素提升宿主适合度的生物测定结果一致,针对参与B族维生素摄取与加工的基因开展的比较转录组分析显示,与携带共生菌的个体相比,无共生菌个体(aposymbiotic)的相关基因表达显著上调;该表达模式与动物发生B族维生素缺乏时的特征相符。然而,通过向昆虫饲料中人工添加B族维生素,或重新感染放线菌共生菌,均可恢复这些基因的正常表达水平。此外,通过在非洲爪蟾(Xenopus laevis)卵母细胞中进行异源表达,对差异表达的硫胺素转运蛋白2(thiamine transporter 2)进行功能鉴定,证实了其在维生素B1的细胞摄取过程中发挥的作用。这些研究结果表明,尽管有益肠道微生物定位于胞外环境,它们仍可成为宿主代谢稳态的关键组成部分,这一特征与定位于菌胞的胞内共生菌的功能特点相似。
创建时间:
2014-09-25



