Sugar signaling modulates SHOOT MERISTEMLESS expression and meristem function in Arabidopsis

• 成果类型: Article
• 署名作者: Lopes, Filipa L.; Jordan, Pau Formosa; Malivert, Alice; Margalha, Leonor; Confraria, Ana; Feil, Regina; Lunn, John E.; Jonsson, Henrik; Landrein, Benoit; Baena-Gonzalez, Elena
• 署名单位: Instituto Gulbenkian de Ciencia; Universidade Nova de Lisboa; University of Cambridge; University of Oxford; Max Planck Society; Centre National de la Recherche Scientifique (CNRS); Ecole Normale Superieure de Lyon (ENS de LYON); Universite Claude Bernard Lyon 1; INRAE; Max Planck Society; University of Cambridge; Lund University
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-11833
• DOI: 10.1073/pnas.240869912
• 发表日期: 2024-09-10
• 关键词: apical meristem; gene-expression; cytokinin; snrk1; activation; thaliana; pathways; protein; stm; tor

摘要

In plants, development of all above- ground tissues relies on the shoot apical meristem (SAM) which balances cell proliferation and differentiation to allow life- long growth. To maximize fitness and survival, meristem activity is adjusted to the prevailing conditions through a poorly understood integration of developmental signals with environmental and nutritional information. Here, we show that sugar signals influence SAM function by altering the protein levels of SHOOT MERISTEMLESS (STM), a key regulator of meristem maintenance. STM is less abundant in inflorescence meristems with lower sugar content, resulting from plants being grown or treated under limiting light conditions. Additionally, sucrose but not light is sufficient to sustain STM accumulation in excised inflorescences. Plants overexpressing the alpha 1- subunit of STM protein under optimal light conditions, despite higher sugar accumulation in the meristem. Furthermore, SnRK1 alpha 1 interacts physically with STM and inhibits its activity in reporter assays, suggesting that SnRK1 represses STM protein function. Contrasting the absence of growth defects in SnRK1 alpha 1 overexpressors, silencing SnRK1 alpha in the SAM leads to meristem dysfunction and severe developmental phenotypes. This is accompanied by reduced STM transcript levels, suggesting indirect effects on STM. Altogether, we demonstrate that sugars promote STM accumulation and that the SnRK1 sugar sensor plays a dual role in the SAM, limiting STM function under unfavorable conditions but being required for overall meristem organization and integrity under favorable conditions. This highlights the importance of sugars and SnRK1 signaling for the proper coordination of meristem activities.