A model of cell-to-cell spread of

Tobacco mosaic virus. Stage I: Upon

infection, viral RNA (vRNA) initiates

synthesis of replicase, plus and minus

vRNA stands, subgenomic RNAs and

movement protein (MP), and coat

protein. In response to infection,

callose accumulates in the wall region

surrounding the plasmodesmata (Pd)

restricting the cytoplasmic sleeve.

Stage II: MP, an integral endoplasmic

reticulum (ER) membrane protein,

functions as a protein raft binding

vRNA on its cytoplasmic domains

forming a replication complex (VRC)

that may also contain replicase.

Intracellular trafficking of the VRC to

the cortical ER is either by diffusion in

the ER lipids (squiggle arrow) or by

vesicular trafficking (open

arrowheads). Stress-induced class I

beta-1,3,glucanase traffics in the

lumen of VRC vesicles to plasma

membrane (PM) with requisite docking

protein (filled arrowheads). Stage III:

Cycling vesicles containing beta-1,3-

glucanase cargo fuse to PM and deliver

beta-1,3-glucanase to the cell wall

(filled arrowheads). Callose is

hydrolyzed, allowing Pd to dilate.

Vesicles with attached VRC recycle

back to the cortical ER, in which

vesicles fuse to cortical ER (curved

arrow). VRC diffuses through the Pd to

adjacent cells by diffusion in ERdesmotubule

continuum (squiggle

arrow) motivated by the concentration

gradient between a viral-infect cell

and adjacent noninfected cells.