Fig. 7.

Schematic of SYT1, VAP27-1, NET3C, and cytoskeletons on the cortical ER. (A) VAP27-1 and NET3C are co-localized on the V-EPCSs, which are surrounded by the S-EPCSs. SYT1 maintains the polygonal network of cortical ER and the stability of V-EPCSs by tethering the ER to the PM. S-EPCSs are often arranged along the actin filament but tend to be excluded by the microtubules. ER-resident VAP27-1 interacts with NET3C and microtubules, whereas NET3C interacts with VAP27-1, ER, and PM membranes, and actin on the V-EPCSs. Therefore, V-EPCSs are stabilized by microtubules, NET3C, and S-EPCSs on the cortical ER. (B) The absence of SYT1 protein results in a less stable and reticulated ER network, fewer V-EPCSs, and less stability of VAP27-1 on the V-EPCSs. The reduced stability of the ER network and the EPCSs may give rise to the stress-sensitive phenotypes in the SYT1 null mutant. (C) Overexpression of VAP27-1 and/or NET3C results in the enlargement of the V-EPCSs, which are encircled by the S-EPCSs. In this model, Arabidopsis ER–PM contact sites can be characterized by a central VAP27-1/NET3C core (V-EPCS) and the SYT1 periphery (S-EPCSs). SYT1 may play roles in creating and maintaining the boundaries of the ER–PM contact sites. (This figure is available in colour at JXB online.)