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Parasitic insect-derived miRNAs modulate host development

Parasitic wasps produce several factors including venom, polydnaviruses (PDVs) and specialized wasp cells named teratocytes that benefit the survival of offspring by altering the physiology of hosts. However, the underlying molecular mechanisms for the alterations remain unclear. Here we find that t...

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Detalles Bibliográficos
Autores principales: Wang, Zhi-zhi, Ye, Xi-qian, Shi, Min, Li, Fei, Wang, Ze-hua, Zhou, Yue-nan, Gu, Qi-juan, Wu, Xiao-tong, Yin, Chuan-lin, Guo, Dian-hao, Hu, Rong-min, Hu, Na-na, Chen, Ting, Zheng, Bo-ying, Zou, Jia-ni, Zhan, Le-qing, Wei, Shu-jun, Wang, Yan-ping, Huang, Jian-hua, Fang, Xiao-dong, Strand, Michael R., Chen, Xue-xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5992160/
https://www.ncbi.nlm.nih.gov/pubmed/29880839
http://dx.doi.org/10.1038/s41467-018-04504-1
Descripción
Sumario:Parasitic wasps produce several factors including venom, polydnaviruses (PDVs) and specialized wasp cells named teratocytes that benefit the survival of offspring by altering the physiology of hosts. However, the underlying molecular mechanisms for the alterations remain unclear. Here we find that the teratocytes of Cotesia vestalis, an endoparasitoid of the diamondback moth Plutella xylostella, and its associated bracovirus (CvBV) can produce miRNAs and deliver the products into the host via different ways. Certain miRNAs in the parasitized host are mainly produced by teratocytes, while the expression level of miRNAs encoded by CvBV can be 100-fold greater in parasitized hosts than non-parasitized ones. We further show that one teratocyte-produced miRNA (Cve-miR-281-3p) and one CvBV-produced miRNA (Cve-miR-novel22-5p-1) arrest host growth by modulating expression of the host ecdysone receptor (EcR). Altogether, our results show the first evidence of cross-species regulation by miRNAs in animal parasitism and their possible function in the alteration of host physiology during parasitism.