1. Implications of the SNARE hypothesis for intracellular membrane topology and dynamics 
James E. Rothman, Graham Warren 
Current Biology 
Volume 4, Issue 3, Pages (March 1994)
DOI: /S (00)

2. Figure 1
The flow pattern of vesicles between the ER and Golgi stack and within the Golgi stack. Anterograde vesicles are known to move from one compartment to the next on the pathway, whereas the flow pattern for retrograde vesicles is unknown. If vesicles return to the ER from all levels of the Golgi stack, a cross-current flow results (a); if they move back from compartment to compartment, mirroring the anterograde flow, the result is a counter-current flow (b).
Current Biology 1994 4, DOI: ( /S (00) )

3. Figure 2
The SNARE hypothesis as applied to transport within the Golgi stack. Each cisterna is postulated to contain a unique type of v-SNARE and t-SNARE. The v-SNARE would be incorporated into budding COP-coated vesicles and would only pair with the t-SNARE in the next cisterna towards the trans side of the stack, leading to heterotypic fusion. The t-SNAREs define the compartment with which vesicles are to fuse, so they have to be excluded from budding vesicles.
Current Biology 1994 4, DOI: ( /S (00) )

4. Figure 3
The SNARE hypothesis can explain the stacking of Golgi cisternae if the v-SNAREs and t-SNAREs that participate in heterotypic fusion (or their close equivalents) can also dock with each other without the prior incorporation of v-SNAREs into COP-coated vesicles. Fusion would be prevented either by a fusion clamp, as indicated in green, or by the involvement of isoforms of the v-SNARE–t-SNARE pair that are unable to trigger fusion.
Current Biology 1994 4, DOI: ( /S (00) )

5. Figure 4
The SNARE hypothesis as applied to homotypic fusion between copies of the same compartment (I and I′ or II and II′). Each compartment contains a unique pair of cognate v-SNAREs and t-SNAREs which trigger homotypic fusion. Both would be excluded from budding transport vesicles.
Current Biology 1994 4, DOI: ( /S (00) )

6. Figure 5
A stochastic mechanism for coated vesicle budding. If periplasmic fusion is triggered simply by the close apposition of lumenal surfaces, there will be no direct coupling between fusion and the mechanical deformation brought about by the assembly of coat subunits. The result would be a scar of varying size that may unavoidably contain resident Golgi proteins. These could diffuse into the coated region after budding.
Current Biology 1994 4, DOI: ( /S (00) )

7. Figure 6
The consequences of periplasmic fusion in (a) tubules and (b) flattened cisternae. Periplasmic fusion within tubules cuts them into smaller tubules. Flattened cisternae become increasingly fenestrated, eventually yielding a tubular reticulum.
Current Biology 1994 4, DOI: ( /S (00) )

8. Figure 7
A classic diagram of the three-dimensional structure of the Golgi complex, as revealed by high-voltage electron microscopy of thick sections. Discrete stacks of cisternae (the compact zone) are linked by tubules (the non-compact zone) that connect equivalent cisternae in adjacent stacks. Note that there are few fenestrations in the central stacked regions but increasing numbers of them towards the rims. The entry (cis) face is highly fenestrated and may be related to the cis-Golgi network [81]. The exit (trans) face is even more highly fenestrated, justifying the terms ‘trans-tubular network’ [79] or ‘trans-Golgi network’ [82] (Figure courtesy of Yves Clermont, adapted from [94]).
Current Biology 1994 4, DOI: ( /S (00) )

9. Figure 8
Freeze-etch images of Golgi membranes. After incubation with cytosol and ATP (a), vesicle budding is restricted to the peripheral fenestrae. After incubation with ATP alone (b), homotypic fusion can no longer repair the damage caused by periplasmic fusion, leading to the generation of large fenestrae that appear at the cisternal rims. The central part of the cisterna is probably armoured against periplasmic fusion by an intercisternal matrix. (Photographs courtesy of John Heuser, reproduced with permission from [80]).
Current Biology 1994 4, DOI: ( /S (00) )

10. Figure 8
Freeze-etch images of Golgi membranes. After incubation with cytosol and ATP (a), vesicle budding is restricted to the peripheral fenestrae. After incubation with ATP alone (b), homotypic fusion can no longer repair the damage caused by periplasmic fusion, leading to the generation of large fenestrae that appear at the cisternal rims. The central part of the cisterna is probably armoured against periplasmic fusion by an intercisternal matrix. (Photographs courtesy of John Heuser, reproduced with permission from [80]).
Current Biology 1994 4, DOI: ( /S (00) )

11. Figure 9
Sorting of embryonic chick cells following re-aggregation of dissociated liver (L), heart (H) and cartilage (C) cells. The liver cells envelop the heart cells which enclose the cartilage cells. This order is determined by the balance of homotypic and heterotypic interactions between the different cell types. (Photograph courtesy of Malcolm Steinberg, reproduced with permission from [95]).
Current Biology 1994 4, DOI: ( /S (00) )