Additional file 4: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Figure S2. Reprogramming efficiency after palmitoyl-CoA and carnitine treatment in early stage (days 1–7). Relative levels of alkaline phosphatase (AP)-positive colonies with or without palmitoyl-CoA (50 μM) + carnitine (50 μM) treatment after reprogramming. Data are presented as the mean ± SEM (n = 3). ***P < 0.005 (Student’s t test). (TIF 72 kb

Additional file 12: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Figure S9. Reprogramming efficiency after GSK3β inhibitor treatment in early stage (days 1–3). Relative levels of alkaline phosphatase (AP)-positive colonies with or without GSK3β inhibitor (CHIR99021, 3 μM) after reprogramming. Data are presented as the mean ± SEM (n = 3). ***P < 0.005 (Student’s t test). (TIF 75 kb

Additional file 1: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Table S1. Primer Sequences. (DOCX 17 kb

Additional file 13: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Figure S10. Western blot results of the phosphorylation of GSK3β. (a) Western blot for phosphorylation of GSK3β in the reprogramming process with or without CPT1 inhibitors (etomoxir (ETO) or PMS). Repeated Western blot 1. (b) Western blot for phosphorylation of GSK3β in the reprogramming process with or without CPT1 inhibitors (ETO or PMS). Repeated Western blot 2. (TIF 376 kb

Additional file 11: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Figure S8. PKC activity and the phosphorylation of GSK3β after Cpt1b overexpression. (a) PKC activity analysis with or without Cpt1b overexpression. (b) Western blot for phosphorylation of GSK3β in the reprogramming process with or without Cpt1b overexpression. Data are presented as the mean ± SEM (n = 3). **P < 0.01 (Student’s t test). (TIF 231 kb

PP2A regulates kinetochore-microtubule attachment during meiosis I in oocyte

<p>Studies using <i>in vitro</i> cultured oocytes have indicated that the protein phosphatase 2A (PP2A), a major serine/threonine protein phosphatase, participates in multiple steps of meiosis. Details of oocyte maturation regulation by PP2A remain unclear and an <i>in vivo</i> model can provide more convincing information. Here, we inactivated PP2A by mutating genes encoding for its catalytic subunits (PP2Acs) in mouse oocytes. We found that eliminating both PP2Acs caused female infertility. Oocytes lacking PP2Acs failed to complete 1^st meiotic division due to chromosome misalignment and abnormal spindle assembly. In mitosis, PP2A counteracts Aurora kinase B/C (AurkB/C) to facilitate correct kinetochore-microtubule (KT-MT) attachment. In meiosis I in oocyte, we found that PP2Ac deficiency destabilized KT-MT attachments. Chemical inhibition of AurkB/C in PP2Ac-null oocytes partly restored the formation of lateral/merotelic KT-MT attachments but not correct KT-MT attachments. Taken together, our findings demonstrate that PP2Acs are essential for chromosome alignments and regulate the formation of correct KT-MT attachments in meiosis I in oocytes.</p

Additional file 7: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Table S2. The pluripotent gene expression of PC-iPSCs. (DOCX 53 kb

Additional file 5: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Figure S3. Reprogramming efficiency of human fibroblasts (HFF-1) after PC treatment (days 1–14). Relative levels of alkaline phosphatase (AP)-positive colonies with or without PC (25 μM) treatment after reprogramming. Data are presented as the mean ± SEM (n = 3). *P < 0.05; ***P < 0.005 (Student’s t test). (TIF 95 kb

Additional file 3: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Figure S1. Protein levels of Cpt1a and Cpt1b in the reprogramming process. (a) Western blot results of Cpt1a and Cpt1b in the reprogramming process at days 7, 14, and 21. (b) Grayscale analysis of Western blot results in (a). (TIF 110 kb

Additional file 9: of Fatty acid oxidation promotes reprogramming by enhancing oxidative phosphorylation and inhibiting protein kinase C

Figure S6. LC-MS results of acyl-CoAs. (a) Positive ion electrospray scan mass spectra of the malonyl-CoA standard. (b) Positive ion electrospray scan mass spectra of the butyl-CoA standard. (c) Positive ion electrospray scan mass spectra of the n-hexanoyl-CoA standard. (d) Positive ion electrospray scan mass spectra of the capryloyl-CoA standard. (e) Positive ion electrospray scan mass spectra of the n-propionyl-CoA standard. (f) Calibration curve of n-propionyl-CoA. (g) Calibration curve of myristoyl-CoA. (h) Calibration curve of lauroyl-CoA. (i) Typical MRM chromatograms of lauroyl-CoA from control and palmitoylcarnitine (PC)-treated groups. (TIF 725 kb