4.8 Article

Distinct mechanisms orchestrate the contra-polarity of IRK and KOIN, two LRR-receptor-kinases controlling root cell division

Journal

NATURE COMMUNICATIONS
Volume 13, Issue 1, Pages -

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41467-021-27913-1

Keywords

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Funding

  1. NSF-GRFP award [DGE-1326120]
  2. Initial Complement (IC) funds from the University of California, Riverside [USDA-NIFA-CA-R-BPS-5156-H]
  3. NSF CAREER award [1751385]
  4. Direct For Biological Sciences [1751385] Funding Source: National Science Foundation
  5. Division Of Integrative Organismal Systems [1751385] Funding Source: National Science Foundation

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Protein polarization is crucial for plant development processes. In this study, the authors demonstrate that IRK and KOIN, two LRR-receptor-kinases in the root meristem, have opposite polarities and rely on distinct mechanisms for polarization. Understanding the mechanisms of protein polarity and its link to cellular functions is important for studying plant development.
Protein polarization coordinates many plant developmental processes. Here the authors show that IRK and KOIN, two LRR-receptor-kinases polarized to opposite sides of cells in the root meristem, rely on distinct mechanisms to achieve polarity. In plants, cell polarity plays key roles in coordinating developmental processes. Despite the characterization of several polarly localized plasma membrane proteins, the mechanisms connecting protein dynamics with cellular functions often remain unclear. Here, we introduce a polarized receptor, KOIN, that restricts cell divisions in the Arabidopsis root meristem. In the endodermis, KOIN polarity is opposite to IRK, a receptor that represses endodermal cell divisions. Their contra-polar localization facilitates dissection of polarity mechanisms and the links between polarity and function. We find that IRK and KOIN are recognized, sorted, and secreted through distinct pathways. IRK extracellular domains determine its polarity and partially rescue the mutant phenotype, whereas KOIN's extracellular domains are insufficient for polar sorting and function. Endodermal expression of an IRK/KOIN chimera generates non-cell-autonomous misregulation of root cell divisions that impacts patterning. Altogether, we reveal two contrasting mechanisms determining these receptors' polarity and link their polarity to cell divisions in root tissue patterning.

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