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#CLV3

2 public questions tagged with this topic.

plant Development -ll

Loss of CLV3 results in:

Loss-of-function clv3 null mutants lack functional CLE peptide ligand, causing derepression, expansion, and ectopic accumulation of WUSCHEL expression domain well beyond organizing center into broader central zone and even peripheral zone. Consequently central zone stem cells overproliferate massively, apical meristem size increases dramatically, peripheral zone generates supernumerary primordia resulting in fasciated stems, enlarged floral meristems producing extra floral organs including stamens and carpels, and club-shaped siliques. Phenotype conclusively shows CLV3 functions as critical brake preventing runaway stem cell accumulation and ensuring proper size control.

Ref: Clark et al., Cell 1995; Lenhard & Laux, Development: clv3 mutants develop enlarged SAM with excess stem cells.

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plant Development -ll

CLAVATA3 (CLV3) in SAM:

CLAVATA3 encodes small secreted CLE peptide family ligand predominantly produced in central zone stem cells of shoot apical meristem, processed into twelve amino acid arabinosylated mature peptide with hydroxylated prolines. It diffuses apoplastically into organizing center where leucine-rich repeat receptor kinases CLV1 homodimer and CLV2-CORYNE heterodimer perceive it activating downstream POLTERGEIST phosphatase and MAPK signaling to repress WUS transcription. This short-range paracrine signal limits WUS domain and stem cell number preventing overproliferation while preserving reservoir required for organ initiation, exemplifying peptide-mediated homeostasis essential for meristem size control.

Ref: Fletcher et al., Science 1999; Laux & Jürgens, Plant Cell: CLV3 maintains stem cell pool via WUS repression.

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