Extended Data Fig. 3: Ablation of Clstn3b impairs adipose thermogenesis.
From: Innervation of thermogenic adipose tissue via a calsyntenin 3β–S100b axis
a–d, Sanger sequencing (a), western blot (b), quantitative PCR (c) (n = 4 mice) and immunofluorescence (d) confirmation of CRISPR–Cas9 deletion of Clstn3b. Scale bars, 10 μm. e, Quantitative PCR analysis of Clstn3 expression in a panel of wild-type mouse tissues, and wild-type and Clstn3b-knockout brain (n = 2 mice for surveying tissue specificity in wild-type mouse; n = 3 mice for wild type and knockout). The primers target the junction between the third and the penultimate exons. f, g, Body weight curve (f) and body composition (g) of wild-type and Clstn3b-knockout mice on chow diet (n = 8 mice). h, Rates of CO2 production from indirect calorimetry analysis of wild-type and Clstn3b-knockout mice (n = 6 mice). i, j, Movement (i) and daily food intake (j) of wild-type and Clstn3b-knockout mice in metabolic chambers (n = 6 mice). k, Oxygen consumption response to acute β3 agonist injection, of wild-type and Clstn3b-knockout mice (n = 6 mice). All data are mean ± s.e.m. Statistical significance was calculated by unpaired Student’s two-sided t-test.
