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Filling in the gaps
In a plant seed, the embryo lies dormant surrounded by nutritive endosperm while awaiting suitable conditions to germinate. A hydrophobic cuticle around the embryo protects it from catastrophic water loss during the early days of growth. Doll et al. identified a back-and-forth signaling pathway that ensures an intact cuticle. The precursor of a signaling peptide is made in the embryo and transferred to the endosperm, where it is processed into an active form. The activated peptide diffuses back into the embryo to activate receptor-like kinases that drive cuticle development. Serve and return continues until all leaks in the cuticle are filled in and the peptide can no longer cross the barrier.
Science, this issue p. 431
Abstract
The plant embryonic cuticle is a hydrophobic barrier deposited de novo by the embryo during seed development. At germination, it protects the seedling from water loss and is, thus, critical for survival. Embryonic cuticle formation is controlled by a signaling pathway involving the ABNORMAL LEAF SHAPE1 subtilase and the two GASSHO receptor-like kinases. We show that a sulfated peptide, TWISTED SEED1 (TWS1), acts as a GASSHO ligand. Cuticle surveillance depends on the action of the subtilase, which, unlike the TWS1 precursor and the GASSHO receptors, is not produced in the embryo but in the neighboring endosperm. Subtilase-mediated processing of the embryo-derived TWS1 precursor releases the active peptide, triggering GASSHO-dependent cuticle reinforcement in the embryo. Thus, a bidirectional molecular dialogue between embryo and endosperm safeguards cuticle integrity before germination.
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