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 α1-subunit of SUCROSE-NON-FERMENTING1-RELATED KINASE 1 (SnRK1) accumulate less STM protein under optimal light conditions, despite higher sugar accumulation in the meristem. Furthermore, SnRK1α1 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 SnRK1α1 overexpressors, silencing SnRK1α 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.

中文翻译：

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糖信号调节拟南芥中的 SHOOT MERISTEMLESS 表达和分生组织功能


在植物中，所有地上组织的发育都依赖于茎尖分生组织（SAM），它平衡细胞增殖和分化以实现终身生长。为了最大限度地提高适应性和生存率，通过对发育信号与环境和营养信息的整合知之甚少，分生组织活动被调整以适应普遍的条件。在这里，我们发现糖信号通过改变分生组织维持的关键调节因子 SHOOT MERISTEMLESS (STM) 的蛋白质水平来影响 SAM 功能。由于植物在有限的光照条件下生长或处理，花序分生组织中的 STM 含量较低，糖含量较低。此外，蔗糖而非光足以维持切下的花序中STM的积累。尽管分生组织中的糖积累较高，但过度表达蔗糖非发酵 1 相关激酶 1 (SnRK1) α1 亚基的植物在最佳光照条件下积累的 STM 蛋白较少。此外，SnRK1α1 与 STM 发生物理相互作用，并在报告基因检测中抑制其活性，表明 SnRK1 抑制 STM 蛋白功能。与 SnRK1α1 过表达细胞不存在生长缺陷相比，沉默 SAM 中的 SnRK1α 会导致分生组织功能障碍和严重的发育表型。这伴随着 STM 转录水平的降低，表明对 STM 的间接影响。总而言之，我们证明糖促进 STM 积累，并且 SnRK1 糖传感器在 SAM 中发挥双重作用，在不利条件下限制 STM 功能，但在有利条件下是整体分生组织和完整性所必需的。这凸显了糖和 SnRK1 信号对于分生组织活动适当协调的重要性。