Plasmodesmata are thought to be key in plant cell–cell communication. These narrow channels cross plant cell walls and connect the cytoplasm of a cell with that of its neighbours. The structure of plasmodesmata has been well characterized, but details of their function and regulation are lacking. A significant feature of plasmodesmata is their size exclusion limit (SEL), which is the maximum size of molecule that can diffuse freely through from one cell to the next. SELs vary spatially and temporally, and they are used to define ‘symplastic domains’; that is, tissues or groups of cells that appear to have functionally equivalent plasmodesmata, allowing certain molecules to move freely throughout that group of cells. Symplastic domains are thought to have important roles in plant development and plant defense.To examine how these domains are set up and regulated, Kim et al. [1xIdentification of a developmental transition in plasmodesmatal function during embryogenesis in Arabidopsis thaliana. Kim, I et al. Development. 2002; 129: 1261–1272PubMedSee all References][1] incubated Arabidopsis thaliana embryos in media containing fluorescent tracer molecules such as HPTS (524 Da) or 10-kDa F-dextran. They identified a new symplastic transition phase, around mid-torpedo stage. Both HPTS and 10- kDa F-dextran could move throughout the whole embryo till the early torpedo stage, but then the SEL of cells seemed to decrease so that 10-kDa F-dextran was no longer transported, but HPTS was still able to move freely throughout.They then screened for mutants in which plasmodesmatal transport was aberrant. They focused their search on embryo defective mutants, reasoning that any significant change to plasmodesmata function would be likely to affect the plant early in development. The screen identified two genes that appear to be involved in regulating the decrease in SEL at the mid-torpedo stage, ISE1 and ISE2 (for ‘increased size exclusion limit of plasmodesmata’). When these genes were mutated, the restricted movement of 10-kDa F-dextrans appeared to be abolished. The mutations caused no other morphological defects (including no obvious effects on plasmodesmata structure), except for a slight developmental retardation and abnormal root hair production. These effects could be a result of failure to restrict the movement of certain molecules. Another possibility is that the morphological changes are the cause of the plasmodesmatal defects, but this is less likely as the authors identified nearly 5000 other mutant lines that had morphological defects but no plasmodesmatal defects.The evidence suggests that the ISE genes are required purely for the regulation of plasmodesmata SELs. If this is so, then their characterization could provide insight into plasmodesmatal regulation and the establishment of symplastic domains. A key question is the level at which the ISE genes function. Do their encoded products interact directly with plasmodesmata, or do they work at a higher level, regulating the change in SEL throughout the whole embryo, for example?
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Jan 1, 2015
Martine Miquel + 3
Open Access