Skip to main content
. 2017 Aug 15;7:8295. doi: 10.1038/s41598-017-07603-z

Figure 6.

Figure 6

Temporal delay in Zpr1 mutation causes phrenic nerve degeneration and defects in synapse formation in Zpr1 ChATMNΔ mice. (a,b) Whole diaphragms from control and Zpr1 ChATMNΔ E18.5 embryos were stained with neurofilament (NF) antibody and α-bungarotoxin (BTX). Image analysis show defects in branching of the phrenic nerve in Zpr1 ChATMNΔ embryos. (cf) Analysis of diaphragms stained with NF and BTX shows defects in the formation of NMJs in mutant embryos. Primary innervation of phrenic nerve was improved in Zpr1 ChATMNΔ compared to Zpr1 Hb9MNΔ mice but reduced numbers of secondary and tertiary branches were generated in Zpr1 ChATMNΔ mice. (gj) Staining of diaphragms with NF and synaptophysin (SYN) shows marked reduction in the tertiary branches and formation of neuromuscular synapses in Zpr1 ChATMNΔ mice. Degeneration of secondary and tertiary branches was detected in mutant embryos (arrows). Lack of terminal branches and functional synapses indicate requirement of ZPR1 in motor neurons for the normal functioning of the respiratory system. Scale bars are 250 μm (a,b), 100 μm (c,d,g,h) and 12.5 μm (e,f,I,j).