miR-142-5p Disrupts Neuronal Morphogenesis Underlying Porcine Hemagglutinating Encephalomyelitis Virus Infection by Targeting Ulk1

Li, Zi; Lan, Yungang; Zhao, Kui; Lv, Xiaoling; Ding, Ning; Lu, Huijun; Zhang, Jing; Yue, Huiqing; Shi, Junchao; Song, Deguang; Gao, Feng; He, Wenqi

In the current study, we discovered that the upregulation of miR-142-5p (Accession number: MIMAT0000154) severely stunted neuronal morphogenesis during PHEV infection by targeting the unc-51-like-kinase1 (Ulk1, NCBI Reference Sequence: NM_009469.3) mRNA 3 ′ untranslated region (3 ′ UTR), which suggested that PHEV largely exploited spatiotemporal control of host microRNAs for neurological disorders. Expression analysis also supported a role for miR-142-5p in the early stages of neuronal development and neurite formation. Further characterization of the downstream mRNAs targeted by miR-142-5p showed that Ulk1, a serine/threonine kinase, is one of the prospective PHEV-regulated mRNAs that are relevant to nerve dysfunction. Thus, we proposed that miR-142-5p-mediated Ulk1 repression might lead to a breakthrough in the understanding of the mechanism of neurological dysfunction induced by PHEV. The results of this study should enhance our collective understanding of how these neurotropic viruses disturb the CNS through post-transcriptional events.