The gene NANA regulates cell proliferation in Arabidopsis thaliana shoot apical meristem without interaction with CLV1, CLV2, CLV3

• Published in: Ontogenez Vol. 45; no. 5; p. 326
• Main Authors: Al'bert, A V, Kavaĭ-ool, U N, Ezhova, T A
• Format: Journal Article
• Language: Russian
• Published: Russia (Federation) 01.09.2014
• Subjects: Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Cell Proliferation; Gene Expression Regulation, Plant - physiology; Genes, Plant; Membrane Proteins - genetics; Meristem - genetics; Meristem - growth & development; Meristem - metabolism; Mutation; Plant Shoots - genetics; Plant Shoots - growth & development; Plant Shoots - metabolism; Plants, Genetically Modified; Protein-Serine-Threonine Kinases; Receptor Protein-Tyrosine Kinases - genetics; Stem Cells - cytology
• ISSN: 0475-1450
• DOI: 10.7868/s0475145014050024

A constancycy of stem cell pool in shoot apical meristem of Arabidopsis thaliana is provided by a genetic regulation system with negative feedback loop based on the interaction of the gene WUS, which maintains indeterminate state of cells, with CLV genes, which restrict the level of WUS expression and stem cell pool size. clv mutations lead to an increase in the pool of stem cells in the apical and floral meristems and wus mutation leads to the opposite effect. Mutation na (nana), like wus mutation, causes premature termination of shoot apical meristem function, although it does not affect the activity of the flower meristem. To elucidate the role of NA in the control of shoot apical meristem functioning, the interaction of NA with CLVgenes were investigated. Additive phenotype of double mutants na clv1, na clv1-1, anl na clv3-2 indicates that the NA gene makes an independent contribution to the functioning of the shoot apical meristem. It is assumed that the NA gene controls apical meristem cell proliferation during the transition to the reproductive phase of plant development, acting much later and independently of the genes WUS-CLV.