Fig. 6: Tsc1 deletion in GABAergic cells causes transient autophagy dysfunctions in adolescent mice. | Nature Communications

Fig. 6: Tsc1 deletion in GABAergic cells causes transient autophagy dysfunctions in adolescent mice.

From: Sensitive period for rescuing parvalbumin interneurons connectivity and social behavior deficits caused by TSC1 loss

Fig. 6

Western blot representative bands of LC3-I, LC3-II (a), p62 proteins (b); pAMPK, AMPK, pULK1, and ULK1 (e). c–g Quantification reveals that LC3-II and pAMPK/AMPK expressions are higher in P14 Tg(Nkx2.1-Cre);Tsc1flox/flox vs Tsc1Ctrl mice (c, f; Unpaired t-test: LC3-II *p = 0.0314; pAMPK/AMPK **p = 0.003), while p62 protein expression was unchanged and pULK1/ULK1 expressions showed a trend towards increased expression (d, g; Unpaired t-test: p62 p = 0.9937; pULK1/ULK1 p = 0.065). h, i Western blot representative bands of LC3-I, LC3-II, p62, pAMPK, and AMPK in adult mice and their quantification (j, k, l) show no differences between the two genotypes (Unpaired t-test: LC3-II p = 0.8446; p62 p = 0.7426; pAMPK/AMPK p = 0.9925). Molecular weight: LC3-I/II :17/14 kDa; p62: 62 kDa; pAMPK: 62 kDa; AMPK: ~62 kDa; ULK1:140 kDa; pULK1: ~150 kDa; GAPDH: 37 kDa. Number of mice at P14: LC3-II; Tsc1Ctrl n = 3, Tg(Nkx2.1-Cre);Tsc1flox/flox n = 3; p62, pAMPK, AMPK, pULK1, ULK1 Tsc1Ctrl n = 4, Tg(Nkx2.1-Cre);Tsc1flox/flox n = 5. Number of mice at P40: LC3-II and p62; Tsc1Ctrl n = 4, Tg(Nkx2.1-Cre);Tsc1flox/flox n = 4; pAMPK and AMPK; Tsc1Ctrl n = 4, Tg(Nkx2.1-Cre);Tsc1flox/flox n = 5. Data represent mean ± SEM. Source data are provided as a Source Data file.

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