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

Based on previous findings, we further explored the basic mechanisms underlying the axon morphology changes caused by PHEV infection. Co-expression of miR-142-5p and Ulk1 was found in the neurite shifts and/or growth cones with a prominent signal in primary neurons (Figure 7A) , which provided evidence for miR-142-5p-mediated Ulk1 repression as a possible explanation for the reduction in axonal elongation. To substantiate this hypothesis, miR-142-5p inhibitors were used to promoting Ulk1 expression in PHEV-infected neurons (Figure 7B) , and we found that miR-142-5p inhibitors efficiently rescued the shortened axon elongations caused by loss function of Ulk1 ( Figure 7C) . Thus, we concluded that Ulk1 mRNA is a downstream element of miR-142-5p in the regulation of axon outgrowth, and that inhibiting miR-142-5p expression in neurons should be able to improve the axon defect caused by PHEV.