<i>Bacillus subtilis</i> STU6 Ameliorates Iron Deficiency in Tomato by Enhancement of Polyamine-Mediated Iron Remobilization

Iron (Fe) deficiency often triggers arginine overproduction in plants. However, it remains elusive whether Fe deficiency-induced increases of arginine levels are involved in beneficial rhizobacteria recruitment and that the mechanism underlying rhizobacteria induced plant Fe deficiency tolerance. Here, Bacillus subtilis STU6 increased soluble Fe content in tomato, thereby alleviating Fe deficiency-induced chlorosis. In a split-root system, STU6 significantly induced arginine exudation by Fe-deficient roots, and increased arginine levels promoted spermidine (Spd) production by STU6 and bacterial colonization. Deletion of the STU6 speB gene inhibited Spd synthesis and abrogated STU6-induced increments of soluble Fe content in the Fe-deficient plants. Increased host Spd levels by STU6 greatly stimulated the NO accumulation in the Fe-deficient roots. Furthermore, disruption of NO signaling markedly repressed STU6-mediated cell wall Fe remobilization. Collectively, our data provide important evidence that chemical dialogues between tomato and STU6 contribute to enhancement of microbe-mediated plant adaptation to Fe deficiency.缺铁（Fe）胁迫常会引发植物体内精氨酸的过量积累。然而，缺铁诱导的精氨酸水平升高是否参与有益根际细菌的招募，以及根际细菌介导植物缺铁耐性的潜在机制，目前仍尚不明确。本研究中，枯草芽孢杆菌（Bacillus subtilis）STU6可提升番茄的可溶性铁含量，从而缓解缺铁诱导的褪绿症状。在分根系统中，STU6显著诱导缺铁根系分泌精氨酸；而精氨酸水平的升高可促进STU6合成亚精胺（Spd），并增强细菌定殖能力。敲除STU6的speB基因会抑制亚精胺的合成，并消除其对缺铁番茄可溶性铁含量的提升作用。STU6介导的宿主亚精胺水平升高，可显著刺激缺铁根系中一氧化氮（NO）的积累。进一步研究发现，阻断一氧化氮信号通路会显著抑制STU6介导的细胞壁铁再动员过程。综上，本研究数据提供了重要证据，表明番茄与STU6之间的化学信号互作，有助于提升微生物介导的植物对缺铁胁迫的适应性。