Figure 2.
Figure 2. Chimeric laminin α5 chain rescues the pre- but not postsynaptic phenotype in Lama5 null mice. (A) Structure of the Mr5G2 transgene, in which the C-terminal three LG domains of laminin α5 are replaced by the corresponding domains of laminin α1. (B) NMJs from control (Lama5+/−;Mr5G2) and Lama5−/−;Mr5G2 sternomastoid at P21 stained as in Fig. 1 B. AChR clusters in the mutant are small and immature but fully occupied by motor neuron terminals. Bar, 10 μm. (C and D) Quantification of topological maturation of AChR clusters (C) and completeness of innervation of AChR clusters (D) in control (Lama5+/−;Mr5G2) and Lama5−/−;Mr5G2 muscles. Counts are from sternomastoid and diaphragm muscles of two animals per genotype, >190 NMJ per animal. *, significant by unpaired t test, P < 0.05.

Chimeric laminin α5 chain rescues the pre- but not postsynaptic phenotype in Lama5 null mice. (A) Structure of the Mr5G2 transgene, in which the C-terminal three LG domains of laminin α5 are replaced by the corresponding domains of laminin α1. (B) NMJs from control (Lama5+/−;Mr5G2) and Lama5−/−;Mr5G2 sternomastoid at P21 stained as in Fig. 1 B. AChR clusters in the mutant are small and immature but fully occupied by motor neuron terminals. Bar, 10 μm. (C and D) Quantification of topological maturation of AChR clusters (C) and completeness of innervation of AChR clusters (D) in control (Lama5+/−;Mr5G2) and Lama5−/−;Mr5G2 muscles. Counts are from sternomastoid and diaphragm muscles of two animals per genotype, >190 NMJ per animal. *, significant by unpaired t test, P < 0.05.

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