National Key Laboratory of Crop Genetic Improvement, Huazhong Agricultural University, Wuhan, China.
Microelement Research Center, College of Resources & Environment, Huazhong Agricultural University, Wuhan, China.
Physiol Plant. 2024 May-Jun;176(3):e14320. doi: 10.1111/ppl.14320.
Many nucleoside triphosphate-diphosphohydrolases (NTPDases/APYRASEs, APYs) play a key role in modulating extracellular nucleotide levels. However, the Golgi-localized APYs, which help control glycosylation, have rarely been studied. Here, we identified AtAPY1, a gene encoding an NTPDase in the Golgi apparatus, which is required for cell wall integrity and plant growth under boron (B) limited availability. Loss of function in AtAPY1 hindered cell elongation and division in root tips while increasing the number of cortical cell layers, leading to swelling of the root tip and abundant root hairs under low B stress. Further, expression pattern analysis revealed that B deficiency significantly induced AtAPY1, especially in the root meristem and stele. Fluorescent-labeled AtAPY1-GFP localized to the Golgi stack. Biochemical analysis showed that AtAPY1 exhibited a preference of UDP and GDP hydrolysis activities. Consequently, the loss of function in AtAPY1 might disturb the homoeostasis of NMP-driven NDP-sugar transport, which was closely related to the synthesis of cell wall polysaccharides. Further, cell wall-composition analysis showed that pectin content increased and borate-dimerized RG-II decreased in apy1 mutants, along with a decrease in cellulose content. Eventually, altered polysaccharide characteristics presumably cause growth defects in apy1 mutants under B deficiency. Altogether, these data strongly support a novel role for AtAPY1 in mediating responses to low B availability by regulating cell wall integrity.
许多核苷三磷酸二磷酸水解酶(NTPDases/APYRASEs,APYs)在调节细胞外核苷酸水平方面发挥着关键作用。然而,很少有研究关注高尔基体定位的 APYs,它们有助于控制糖基化。在这里,我们鉴定了 AtAPY1,它是编码高尔基体中 NTPDase 的基因,该基因对于细胞壁完整性和植物在硼(B)有限供应下的生长是必需的。AtAPY1 功能丧失会阻碍根尖细胞的伸长和分裂,同时增加皮层细胞层数,导致根尖肿胀和根毛丰富,在低 B 胁迫下。此外,表达模式分析表明,B 缺乏显著诱导 AtAPY1 的表达,特别是在根分生组织和中柱。荧光标记的 AtAPY1-GFP 定位于高尔基堆栈。生化分析表明,AtAPY1 表现出对 UDP 和 GDP 水解活性的偏好。因此,AtAPY1 的功能丧失可能会扰乱 NMP 驱动的 NDP-糖转运的动态平衡,这与细胞壁多糖的合成密切相关。此外,细胞壁成分分析表明,果胶含量增加,硼二聚 RG-II 减少,纤维素含量减少。最终,在 B 缺乏下,改变的多糖特性可能导致 apy1 突变体的生长缺陷。总之,这些数据有力地支持了 AtAPY1 通过调节细胞壁完整性来介导对低 B 供应的响应的新作用。