Genome-wide transcriptional response of silkworm (Bombyx mori) to infection by the microsporidian Nosema bombycis.

Genome-wide transcriptional response of silkworm (Bombyx mori) to infection by the microsporidian Nosema bombycis.
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家蚕(Bombyx mori)对家蚕微孢子虫感染的全基因组转录反应

DOI:
10.1371/journal.pone.0084137
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Zhou Z
Zhou Z
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Ma Z;Li C;Pan G;Li Z;Han B;Xu J;Lan X;Chen J;Yang D;Chen Q;Sang Q;Ji X;Li T;Long M;Zhou Z

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微孢子虫由于能感染从原生生物到哺乳动物等多种物种,包括艾滋病或癌症导致免疫功能低下的患者,因而备受关注。除了对蜜蜂微孢子虫(Nosema ceranae)的研究外,很少有研究致力于阐明宿主对微孢子虫感染的反应机制。家蚕微孢子虫(Nosema bombycis)是家蚕微粒子病的病原体,给蚕业造成巨大经济损失。详细了解家蚕(Bombyx mori)对家蚕微孢子虫感染的反应有助于预防这种疾病。对家蚕在感染家蚕微孢子虫后2、4、6和8天的基因表达谱进行了全基因组调查,结果显示分别有64、244、1328、1887个基因被诱导。多达124个参与基础代谢途径的基因被调控。值得注意的是,在家蚕中参与保幼激素合成和代谢途径的基因被诱导,这表明宿主可能会积累保幼激素以应对感染。有趣的是,家蚕微孢子虫能够抑制家蚕血淋巴中的丝氨酸蛋白酶级联黑化途径,这可能是由于微孢子虫分泌丝氨酸蛋白酶抑制剂(serpins)所致。家蚕微孢子虫还诱导了几种细胞免疫因子的上调,其中CTL11被认为参与孢子识别和免疫信号转导。基因芯片和实时定量PCR分析表明家蚕的Toll和JAK/STAT途径被激活。抗菌肽(包括格洛弗林、莱博辛和莫里辛)显著上调,有力地表明抗菌肽防御机制被触发以抵抗入侵的微孢子虫。对家蚕微孢子虫特异性反应因子的分析表明它们在抗微孢子虫防御中具有重要作用。总体而言,这项研究初步深入了解了家蚕和家蚕微孢子虫之间宿主 - 寄生虫相互作用的潜在分子机制,并可能为进一步研究昆虫和微孢子虫之间的宿主 - 寄生虫相互作用奠定基础。
Microsporidia have attracted much attention because they infect a variety of species ranging from protists to mammals, including immunocompromised patients with AIDS or cancer. Aside from the study on Nosema ceranae, few works have focused on elucidating the mechanism in host response to microsporidia infection. Nosema bombycis is a pathogen of silkworm pébrine that causes great economic losses to the silkworm industry. Detailed understanding of the host (Bombyx mori) response to infection by N. bombycis is helpful for prevention of this disease. A genome-wide survey of the gene expression profile at 2, 4, 6 and 8 days post-infection by N. bombycis was performed and results showed that 64, 244, 1,328, 1,887 genes were induced, respectively. Up to 124 genes, which are involved in basal metabolism pathways, were modulated. Notably, B. mori genes that play a role in juvenile hormone synthesis and metabolism pathways were induced, suggesting that the host may accumulate JH as a response to infection. Interestingly, N. bombycis can inhibit the silkworm serine protease cascade melanization pathway in hemolymph, which may be due to the secretion of serpins in the microsporidia. N. bombycis also induced up-regulation of several cellular immune factors, in which CTL11 has been suggested to be involved in both spore recognition and immune signal transduction. Microarray and real-time PCR analysis indicated the activation of silkworm Toll and JAK/STAT pathways. The notable up-regulation of antimicrobial peptides, including gloverins, lebocins and moricins, strongly indicated that antimicrobial peptide defense mechanisms were triggered to resist the invasive microsporidia. An analysis of N. bombycis-specific response factors suggested their important roles in anti-microsporidia defense. Overall, this study primarily provides insight into the potential molecular mechanisms for the host-parasite interaction between B. mori and N. bombycis and may provide a foundation for further work on host-parasite interaction between insects and microsporidia.
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