Figure 1 | Scientific Reports

Figure 1

From: Lack of Cathepsin D in the central nervous system results in microglia and astrocyte activation and the accumulation of proteinopathy-related proteins

Figure 1

CtsD-Nes mice show stunted growth and neurological dysfunction. (A) Genotyping of CtsD-CKO (CtsDflox/flox; Nestin-Cre) mice. “F” in the upper panel indicates CtsD-floxed alleles (about 800 bp), and “+” indicates wild type alleles (about 700 bp). In the lower panel, “+” indicates Nestin-Cre transgenes (about 900 bp). (B) Representative image of immunoblotting of CtsD in whole brain lysates from the CtsD-CKO and control littermate mice at p14. Molecular masses of pro-cathepsin D (about 46 kDa) and mature cathepsin D (about 28 kDa) are decreased in CtsD-CKO brain lysates. As a loading control in each well, ß-actin is detected using anti- ß-actin antibody. (C–E) Physiological findings of a 32-day-old CtsD-CKO mouse. The CtsD-CKO mouse is smaller in size than the control littermate mouse (C), and shows a kinetic epilepsy-like phenotype (D). The size of the brain of CtsD-CKO mouse was smaller than that of the control littermate mouse (E). (F) Growth defect of CtsD-CKO mice (**p < 0.03, ***p < 0.001, n = three to eleven mice from each genotype mouse.). "Control" indicates CtsDflox/flox mouse, and “CtsD-CKO” indicates CtsDflox/flox; Nestin-Cre mouse. Supplementary Fig. 7 shows uncropped PCR banding patterns and blots.

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