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CYSTEINE-RICH RLK2 regulates development via callose synthase-dependent symplastic transport in Arabidopsis

2026/06/29 by Adam Zeiner, Julia Krasensky-Wrzaczek, Sunita Jindal +12 · 2 voices
Agricultural and Biological Sciences · #Plant Molecular Biology Research #Plant nutrient uptake and metabolism #Plant responses to water stress

paper · doi:10.1093/plphys/kiag453

openalex publication_date 2026/06/29 · openalex created_date 2026/06/30 · openalex updated_date 2026/07/22

Abstract

Abstract CYSTEINE-RICH RECEPTOR-LIKE PROTEIN KINASEs (CRKs) play an important role in plant development and stress responses. One of the best described members of the Arabidopsis CRK family is CRK2, which was proposed as a crucial regulator of intercellular transport facilitated by plasmodesmata (PD). As intercellular channels allowing symplastic communication, PD-mediated transport is predominantly regulated by callose synthase (CALS)-mediated callose deposition. This process can impact not just the distribution of molecules between adjacent cells, but also the symplastic loading of vascular tissue, thereby influencing plant stress responses and developmental processes. Here we described the overlapping expression pattern of genes encoding phylogenetically closely related CALS1 and CALS3. Both CALSs were phosphorylated in vitro by CRK2, and the genetic interaction between genes encoding CRK2 and CALS1 or CALS3 revealed their impact on callose deposition, rosette growth, primary root length, and development, represented as a decreased number of true leaves. Importantly, we observed significant accumulation of starch in crk2 mutant plants, especially in developmentally older leaves, which was reverted by the independent introduction of cals1.5 and cals3.1 into the crk2 mutant background. The observed starch accumulation was accompanied by photosynthesis inhibition. We propose that the growth and developmental alterations of crk2 are caused by decreased phloem loading, which resulted in starch accumulation in source organs, and subsequent sink tissue starvation. Our results propose CRK2 as negative regulator of CALS1 and CALS3 regulating source to sink transport, which impacts plant growth and development.

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