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. 2019 Dec 23;16(11):1932–1948. doi: 10.1080/15548627.2019.1705007

Figure 2.

Figure 2.

Basal autophagy is independent of MTOR activity in podocytes in vivo. (A) Schematic of generating podocyte-specific deletion of Rptor or Tsc1 using Nphs2-Cre mice and Cre-Lox technique. (B) Cryosections from 2-week-old mice bearing podocyte-specific knockout for Rptor and transgenic for Gfp-Lc3 compared to Gfp-Lc3 WT mice (NID1 in red, GFP-LC3 in green). (C) Quantification of GFP-LC3 autophagosomes per glomerular area out of 30 glomeruli each from 3 mice (ns, not significant). (D) Cryosections from 2-week-old mice bearing podocyte-specific knockout for Tsc1 and transgenic for Gfp-Lc3 compared to Gfp-Lc3 WT mice (NID1 in red, GFP-LC3 in green). (E) Quantification of GFP-LC3 autophagosomes per glomerular area out of 30 glomeruli each from 3 mice (ns, not significant). (F) Western blot out of glomerular lysates obtained from 2-week-old mice for MTORC1 downstream targets and LC3 and SQSTM1 abundance. (G) Densitometry for LC3-II, SQSTM1 and p-RPS6 obtained from 3 WT glomerular lysates and 3 glomerular lysates obtained from 2-week-old mice bearing a podocyte-specific deletion of Rptor or Tsc1, respectively (** ≤ 0.01, * ≤ 0.05, ns, not significant)