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转运蛋白 NRT1.5/NPF7.3 通过调控 PIN-FORMED2 的降解来抑制低钾胁迫下主根的生长。

Transporter NRT1.5/NPF7.3 suppresses primary root growth under low K stress by regulating the degradation of PIN-FORMED2.

机构信息

Jiangsu Key Laboratory for Biodiversity and Biotechnology, College of Life Sciences, Nanjing Normal University, Nanjing, 210023, China.

出版信息

BMC Plant Biol. 2022 Jul 8;22(1):330. doi: 10.1186/s12870-022-03730-6.

Abstract

BACKGROUND

The availability of potassium is one of the main environmental factors for modifying the plasticity of root architecture. Many potassium channels and transporters are involved in regulating primary root growth in response to low potassium stress. NRT1.5/NPF7.3 transporter is a NO/H and K/H cotransporter, and participates in NO and K translocation from the roots to the shoots. However, the underlying mechanism of NRT1.5-regulated primary root growth under low potassium stress is unclear.

RESULTS

We show that NRT1.5/NPF7.3 inhibited primary root growth under low potassium conditions by regulating the accumulation of PIN2 protein and auxin levels. Under low potassium conditions, the mutants nrt1.5 and lks2 exhibited longer primary roots, longer meristem regions and elongation zones of primary roots, and more cell activity in the meristem region compared to WT plants, revealing the involvement of NRT1.5 in LK (low potassium)-inhibition primary root growth. In addition, exogenous auxin (IAA), auxin analogue (NAA, 2.4-D) or auxin precursor (IBA) promoted the primary root growth of WT and the complementation line NRT1.5 COM plants. In addition, the application of NPA inhibited the primary root growth of the nrt1.5 and lks2 mutants. Auxin accumulation was higher in the root tip of nrt1.5 plants than in WT plants, indicating that NRT1.5 regulates root growth inhibition by regulating auxin distribution. Furthermore, PIN2 was degraded more quickly in nrt1.5 plants under LK stress.

CONCLUSIONS

Our findings reveal that NRT1.5 inhibits primary root growth by modulating the auxin level in the root tip via the degradation of PIN2.

摘要

背景

钾的可利用性是改变根系可塑性的主要环境因素之一。许多钾通道和转运蛋白参与调节主根生长以响应低钾胁迫。NRT1.5/NPF7.3 转运蛋白是一种 NO/H 和 K/H 共转运蛋白,参与从根部向地上部转运 NO 和 K。然而,NRT1.5 调节低钾胁迫下主根生长的潜在机制尚不清楚。

结果

我们表明,NRT1.5/NPF7.3 通过调节 PIN2 蛋白和生长素水平来抑制低钾条件下的主根生长。在低钾条件下,突变体 nrt1.5 和 lks2 表现出较长的主根、较长的分生组织区域和主根伸长区,以及分生组织区域中更多的细胞活性,表明 NRT1.5 参与 LK(低钾)抑制主根生长。此外,外源性生长素(IAA)、生长素类似物(NAA、2.4-D)或生长素前体(IBA)促进了 WT 和互补系 NRT1.5 COM 植物的主根生长。此外,NPA 的应用抑制了 nrt1.5 和 lks2 突变体的主根生长。nrt1.5 植物根尖生长素积累高于 WT 植物,表明 NRT1.5 通过调节生长素分布来调节根生长抑制。此外,在低钾胁迫下,nrt1.5 植物中 PIN2 降解更快。

结论

我们的研究结果表明,NRT1.5 通过降解 PIN2 来调节根尖生长素水平来抑制主根生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7202/9264542/ed2906b3c784/12870_2022_3730_Fig1_HTML.jpg

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