A proposed model showing that PDLP7 facilitates PD opening or closure via callose degradation. (IMAGE)
Caption
In WT, PDLP7 interacts with BG10 through its GnK2-1 domain to restrict BG10 from hydrolyzing callose. Free callose in the cell wall is deposited at the PD neck to maintain a dynamically balanced steady state of callose (Fig.a). In the pdlp7 mutant, the absence of PLDP7 leads to increased BG10 activity, resulting in decreased callose content at the PD neck and ultimately to PD opening (Fig.b). When virus attack or in the PDLP7 OE lines, the highly expressed PDLP7 interacts with BG10, potentially inhibiting BG10 from hydrolyzing callose. As a result, more callose is deposited into the neck of the cell wall, effectively sealing off the plasmodesmata and providing resistance against the virus ((Fig.c).
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