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Ac34 inhibits CRM1-dependent nuclear export during AcMNPV infection.

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posted on 2016-11-01, 04:30 authored by Jingfang Mu, Yongli Zhang, Yangyang Hu, Xue Hu, Yuan Zhou, He Zhao, Rongjuan Pei, Chunchen Wu, Jizheng Chen, Han Zhao, Kai Yang, Monique M. van Oers, Xinwen Chen, Yun Wang

(A). Ac34 is sufficient to inhibit CRM1-dependent nuclear export. EGFP-NES was co-expressed with mCherry, mC-Ac34, or mC-Ac341-195 in Sf9 cells. In cells co-expressing EGFP-NES and mCherry (row 1 and 2), ethanol (1 μl) or LMB (0.1 μg/ml) was added to the culture medium at 44 hpt. At 48 hpt, all the cells were fixed and subjected to fluorescence microscopy assays. (B). Ac34 is involved in AcMNPV-induced CRM1 pathway dysfunction. A mCherry-NES encoding plasmid was co-transfected with the indicated bacmids in Sf9 cells. At 48 hpt, all the cells were fixed and subjected to fluorescence microscopy assays. The arrow pointed to the bacmid-free cells that showed different spatial pattern of mCherry-NES in comparison with the adjacent vAc34KOac34 transfected cells. Densitometry assays were performed simultaneously. The bars represent the means and standard errors of the means for three independent experiments. Each experiment involves the quantification of 30 transfected cells. Scale bar: 20 μm. ***, P<0.001, **, P<0.01 *, P<0.05.

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