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. 2010 Feb 9;107(11):5076–5081. doi: 10.1073/pnas.0908790107

Fig. 4.

Fig. 4.

Abnormal cerebellar morphology in Lmnb2−/− mice. (A) Cross-sections of cerebellum in newborn WT and Lmnb2−/− mice. The cerebellum of Lmnb2−/− embryos was smooth and smaller in size; asterisks show fissures in the WT cerebellum (absent in the Lmnb2−/− cerebellum). (B) Cerebellar sections of E19.5 WT and Lmnb2−/− embryos stained with H&E (Top) and with an antibody against calbindin (Bottom). Calbindin stains the layer of Purkinje cells (arrow in WT section; layer is also visible in the H&E-stained section). Note the reduced thickness of the external granule layer in Lmnb2−/− cerebellum (arrowhead). Cp, choroid plexus. (C) Cross-section of the cerebellum from an E16.5 Lmnb2+/− embryo and a newborn Lmnb2+/− mouse (P0) after whole-mount staining for β-galactosidase. Lmnb2 expression is noted in the superficial layer of the cerebellum, the external granule layer (arrowhead) and in the vicinity of the Purkinje cell layer (arrow). (D) Immunostaining of a cerebellar section of an E17.5 Lmnb2+/− embryo with antibodies against lamin B1 (green) and lamin B2 (red). Nuclear DNA was stained with DAPI. Lamins B1 and B2 are detected in all cells, with a stronger signal in the Purkinje layer (arrow).