Abstract The precise regulation of stem cells in the shoot apical meristems (SAMs) involves the function of the homeodomain transcription factor (TF)‐WUSCHEL (WUS). WUS has been shown to move from the site of production‐the rib‐meristem (RM), into overlaying cells of the central zone (CZ), where it specifies stem cells and also regulates the transcription ofCLAVATA3 (CLV3). The secreted signalling peptide CLV3 activates a receptor kinase signalling that restrictsWUStranscription and also regulates the nuclear gradient of WUS by offsetting nuclear export. WUS has been shown to regulate bothCLV3levels and spatial activation, restricting its expression to a few cells in the CZ. The HAIRY MERISTEM (HAM), a GRASS‐domain class of TFs expressed in the RM, has been shown to physically interact with WUS and regulateCLV3expression. However, the mechanisms by which this interaction regulatesCLV3expression non‐cell autonomously remain unclear. Here, we show that HAM function is required for regulating the WUS protein stability, and theCLV3expression responds to altered WUS protein levels inhammutants. Thus, HAM proteins non‐cell autonomously regulatesCLV3expression.
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This content will become publicly available on July 1, 2026
Floral innovation through modifications in stem cell peptide signaling
Abstract Understanding how evolution shapes genetic networks to create new developmental forms is a central question in biology. Flowering shoot (inflorescence) architecture varies significantly across plant families and is a key target of genetic engineering efforts in many crops1–4. Asteraceae (sunflower family), comprising 10% of flowering plants, all have capitula, a novel inflorescence that mimics a single flower5,6. Asteraceae capitula are highly diverse but are thought to have evolved once via unknown mechanisms7,8. During capitulum development, shoot stem cells undergo prolonged proliferation to accommodate the formation of intersecting spirals of flowers (florets) along the disk-shaped head9,10. Here we show that capitulum evolution paralleled decreases in CLAVATA3 (CLV3) peptide signaling, a conserved repressor of stem cell proliferation. We trace this to novel amino acid changes in the mature CLV3 peptide which decrease receptor binding and downstream transcriptional outputs. Using genetically tractable Asteraceae models, we show that reversion ofCLV3to a more active form impairs Asteraceae stem cell regulation and capitulum development. Additionally, we trace the evolution ofCLV3and its receptors across the Asterales allowing inferences on capitulum evolution within this lineage. Our findings reveal novel mechanisms driving evolutionary innovation in plant reproduction and suggest new approaches for genetic engineering in crop species.
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- PAR ID:
- 10645329
- Publisher / Repository:
- bioRxiv
- Date Published:
- Format(s):
- Medium: X
- Institution:
- Clemson University
- Sponsoring Org:
- National Science Foundation
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