Another explanation for whorl formation is the presence of one or more abundant ER-associated proteins that stabilize stacked ER membranes in the absence of ongoing protein synthesis. Support for this model comes from studies in cultured cells showing that protein overexpression can induce ER whorl formation. Snapp et al. (2003) [15] reported that overexpression of cytochrome b5 induced the formation of smooth ER whorls, they called organized smooth ER (OSER), in transfected CV-1 cells. These same OSER structures could be observed when b5-GFP fusion proteins were over expressed, as long as they retained dimerization function in either the b5 or GFP protein domains. The authors proposed that weak noncovalent interactions between ER resident proteins on apposing stacked membranes are sufficient to maintain smooth ER whorl structures. Similar OSER structures were shown to form in HeLa cells that were infected with an adenovirus vector expressing the ER resident protein LAT linked to a heterologous protein dimerization domain [16] , or overexpression of a viral protein that associates with ER membranes in infected cells [17] .