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. 2003 Jan 15;23(2):392–402. doi: 10.1523/JNEUROSCI.23-02-00392.2003

Fig. 9.

Fig. 9.

The intracellular juxtamembrane domain of β-dystroglycan contains an inhibitory element. Transfected myotubes were treated for 5 hr with 250 pm agrin N2(4,8) and double-labeled for AChRs (Texas Red-conjugated α-bungarotoxin;B, D, F) and anti-HA immunoreactivity (FITC-conjugated anti-mouse IgG; A, C, E).A and B are a CD8tm-transfected myotube.C and D are a DGtm-transfected myotube.E and F are a CD8tmDGJK-transfected myotube. G, Quantification of agrin- induced AChR clustering in myotubes transfected with β-dystroglycan and CD8 transmembrane constructs with and without the cytosolic juxtamembrane domain (mean ± SEM; n= 8). Removal of four amino acids (KRKG) from DGtmJ (DGtm) restores AChR clustering to control values. The corresponding CD8 mutants (CD8tmJ and CD8tm) are not statistically different, whereas the chimeras CD8tmDGJ and CD8tmDGJK cause inhibition.Asterisks indicate mean values that are statistically different from CD8tmJ (p < 0.05; Student's t test). Inset, Anti-HA Western blot of COS cells transiently transfected with no DNA (1), DGtm (2), CD8tm (3), CD8tmJ (4), or CD8tmDGJ (5). Samples were separated by 16% SDS-PAGE. Arrows indicate molecular weight standards (×103): 6, 3. Scale bar, 50 μm.