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. 2018 Dec 14;7:e41050. doi: 10.7554/eLife.41050

Figure 2. δ-Pcdhs mediate homophilic aggregation.

(A) Aggregates formed by ECTM constructs tagged with P2A-GFP. Pcdh11x could not be expressed. Scale bar, 100 μm. (B) Distribution of aggregate sizes after titrating DNA input. Results for each δ-Pcdh were determined from three independent electroporations. Pcdh10 aggregate size could not be increased by varying DNA input. (C) Pair wise analysis of δ-Pcdh binding specificity. Only pairs expressing the same δ-Pcdh coaggregated (diagonal), while cells expressing different δ-Pcdhs segregated. Results for each pair were determined from two independent electroporations. Scale bar, 100 μm.

Figure 2.

Figure 2—figure supplement 1. δ-Pcdh homophilic aggregation does not require an intracellular domain and is sensitive to EDTA.

Figure 2—figure supplement 1.

(A) Representative images of aggregates induced by a Pcdh1 ECTM construct (left) and a full length Pcdh1 construct (middle). The two populations coaggregated when mixed (right), demonstrating the intracellular domain is not required for homophilic recognition and adhesion. Scale bar, 100 μm. (B) δ-Pcdhs are localized at sites of intercellular adhesion (arrowhead). K562 cells expressing Pcdh7-RFP were fixed and stained with DAPI prior to imaging. Scale bar, 10 μm. (C) δ-Pcdh aggregation is severely disrupted by the presence of 20 μM EDTA, although some δ-Pcdhs still maintained small aggregates (e.g. Pcdh8 and Pcdh17). Scale bar, 100 μm.