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Fig. 4 Pmpcb deficiency leads to increased cell apoptosis and increased DNA damage in proliferation cells in CNS. A WB analysis of P53 and Caspase3 in WT siblings and pmpcb−/− larvae at 72 hpf (A, left), and the calculation of the relatively translational levels of P53 and Caspase3 (17 kDa) (A, right). B Bcl-2 protein level in WT siblings and pmpcb−/− larvae at 72 hpf (B, left), and the calculation of the relatively translational level of Bcl-2 (B, right). C, D Edu and H2AX co-staining in brain sections from WT siblings and pmpcb−/− larvae at 72 hpf (C, left), with the calculation data of the number of Edu+H2AX+ cells (C, right) and the relative fluorescence intensity (D). E, F Edu, TUNEL, and Sox2 co-staining in brain sections from WT siblings and pmpcb−/− larvae at 72 hpf (E, left), with the calculation data of the number of Edu+TUNEL+Sox2+ cells (E, right) and the relative fluorescence intensity (F). G Transcriptional expression of the mature glial cell markers gfap and vimentin in the WT siblings, WT siblings injected with p53 morpholinos (MOs), pmpcb−/− mutants and the pmpcb.−/− mutants injected with p53 MOs at 72 hpf (G, left). G, right, Calculation of gfap and vimentin expression levels in different samples. G, lateral view, anterior to the left, and dorsal to the up. Each experiment was repeated at least three times, and a representative result is shown. Data are analyzed using GraphPad Prism 9.5 for t-test, and are presented as mean ± SD. ***P < 0.001, **P < 0.01, ns, not significant. Scale bar, 200 μm (G), 50 μm (C, E), 25 μm (E, Enlarged)