Plasmodesmata act as key elements in intercellular communication, coordinating processes related to plant growth, development, and responses to environmental stresses. While many of the developmental, biotic, and abiotic signals are primarily perceived at the plasma membrane (PM) by receptor proteins, plasmodesmata also cluster receptor-like activities; whether these two pathways interact is currently unknown. Here we show that specific PM-located Leucine-Rich-Repeat Receptor-Like-Kinases (LRR-RLKs), QSK1 and IMK2, which under optimal growth conditions are absent from plasmodesmata, rapidly relocate and cluster to the pores in response to osmotic stress. This process is remarkably fast, is not a general feature of PM-associated proteins, and is independent of sterol- and sphingolipid- membrane composition. Focusing on QSK1, previously reported to be involved in stress responses, we show that relocalisation in response to mannitol depends on QSK1 phosphorylation. Loss-of-function mutation in QSK1 results in delayed lateral root (LR) development and the mutant is affected in the root response to mannitol stress. Callose-mediated plasmodesmata regulation is known to regulate LR development. We found that callose levels are reduced in the qsk1 mutant background with a root phenotype resembling ectopic expression of PdBG1, an enzyme that degrades callose at the pores. Both the LR and callose phenotypes can be complemented by expression of wild-type and phosphomimic QSK1 variants, but not by phosphodead QSK1 mutant which fails to relocalise at plasmodesmata. Together the data indicate that re-organisation of RLKs to plasmodesmata is important for the regulation of callose and LR development as part of the plant response to osmotic stress.
CORE (COnnecting REpositories)
CORE (COnnecting REpositories)