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. 2018 Apr 18;9:1544. doi: 10.1038/s41467-018-03796-7

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Selective deletion of TAp63 in POMC neurons impairs neural activities of POMC neurons. a Firing rate, recorded by the whole-cell patch clamp, in POMC neurons from male and female mice, with or without POMC-specific TAp63 deletion, that have been fed with HFD for 4 weeks. Data are presented as mean ± SEM with individual data points. N = 15–26 per group. *P < 0.05 between male and female with the same genotype; ^#P < 0.05 between the two genotypes with the same sex in two-way ANOVA followed by post hoc Sidak tests. b Resting membrane potential, recorded by the perforated patch clamp, in POMC neurons from male and female mice, with or without POMC-specific TAp63 deletion, that have been fed with HFD for 4 weeks. Data are presented as mean ± SEM with individual data points. N = 22–39 per group. *P < 0.05 between male and female with the same genotype; ^#P < 0.05 between the two genotypes with the same sex in two-way ANOVA followed by post hoc Sidak tests. c Typical mIPSC recorded from the POMC neurons of control male, control female, or pomc-TAp63 KO female mice that have been fed with HFD for 4 weeks. d, e Amplitude (d) and frequency (e) of mIPSC in POMC neurons. Data are presented as mean ± SEM with individual data points. N = 10–17 per group. **P < 0.01 or ***P < 0.001 in one-way ANOVA followed by Sidak tests. f, g Percentage of POMC neurons from control and pomc-TAp63 KO mice that were activated by PPT. PPT-induced activation was defined as either > 20% increases in firing rate (f) or by > 2 mV depolarization (g). h Fluorescence for TOMATO (left) and ZsGreen (middle), and bright-field illumination (right) of a recorded ERα-positive POMC neuron in a brain slice prepared from ERα-ZsGreen/POMC-CreER^T2/Rosa26-tdTOMATO mouse with tamoxifen induction at 11 weeks of age. i Representative current clamp traces for PPT-induced responses in ERα-positive POMC neurons from control or pomc-TAp63 KO mice. j, k PPT-induced depolarization (j) and increases in firing rate (k) in ERα-positive POMC neurons from control or pomc-TAp63 KO mice. Data are presented as mean ± SEM. N = 10–14 per group. *P < 0.05 or **P < 0.01 in t-tests