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. 2016 Apr 26;6:25153. doi: 10.1038/srep25153

Figure 6. Foci formations of EB1 and EB2 were regulated by PINK1-Parkin.

Figure 6

(A,B) The formation of EB family protein foci was abolished in Pink1- and Parkin-deficient cells. The indicated proteins were co-expressed in Parkin+/+ (wild type [WT]), Parkin−/− (knockout [KO]), and PINK1-knockdown MEFs, and cells were treated with 30 μM CCCP for 12 h. Microscopic images are shown in panel (A), red, blue and purple column represent EB1, EB2 and EB1EB2 respectively. Scale bar, 10 μm. The number of foci is shown in panel (B). Statistical significance was determined using t test (n = 19, mean ± SD, **P < 0.01). (C–D) Parkin translocation to fragmented mitochondria in EB2 KD cells in response to CCCP treatment. Parkin-GFP and mitochondria-DsRed were co-expressed in NC and EB2 KD cells, and cells were treated with CCCP for 9 h. Microscopic images are shown in panel (C). Scale bar, 10 μm. Histogram shows Pearson’s coefficient between Parkin and damaged mitochondria in WT or EB2 KD cells in panel (D). Statistical significance was determined by using t test. n.s. represents for no significant difference. (E) Timm23 degradation was significantly limited in Parkin−/− MEFs and PINK1 KD MEFs in response to CCCP treatment. Indicated cells were treated with or without CCCP as shown. Cells were then subjected to immunoblot analysis using the indicated antibodies. (F) Parkin and PINK1 expression levels in Parkin−/− and PINK1 KD cells were examined by immunoblotting.