Abstract
Unlike most animals, higher plants continue to generate new organs post-embryonically from stem cells located within shoot, root and floral meristems. These stem cells are not permanent initials, but instead are positionally determined. Therefore, meristem maintenance depends upon a balance between stem cell division within the meristem center and differentiation toward the periphery. In the shoot apical meristem (SAM) of Arabidopsis thaliana, this balance is partly regulated by the signaling molecules CLAVATA1 (CLV1), a receptor protein kinase, and CLV3, a putative extracellular protein. Loss-of-function CLV1 and CLV3 mutants accumulate stem cells, resulting in meristem enlargement. Although genetic data suggests CLV1 and CLV3 act in the same signaling pathway, expression studies reveal that the two genes are expressed in different cell layers within the SAM. One model for their activity is that secreted CLV3 binds to the plasma membrane-associated CLV1 complex to limit stem cell accumulation either by decreasing stem cell division or increasing differentiation. Two recent papers1,2 support this role for CLV1 and CLV3 as a receptor and ligand pair negatively regulating SAM stem cell proliferation.
Published Version
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