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拟南芥中的肿瘤发育涉及类摇床型钾离子通道AKT1和AKT2/3。

Tumour development in Arabidopsis thaliana involves the Shaker-like K+ channels AKT1 and AKT2/3.

作者信息

Deeken Rosalia, Ivashikina Natalya, Czirjak Tina, Philippar Katrin, Becker Dirk, Ache Peter, Hedrich Rainer

机构信息

Julius-von-Sachs-Institut für Molekulare Pflanzenphysiologie und Biophysik, Universität Würzburg, Julius-von-Sachs-Platz 2, D-97082 Würzburg, Germany.

出版信息

Plant J. 2003 Jun;34(6):778-87. doi: 10.1046/j.1365-313x.2003.01766.x.

Abstract

After completion of the Arabidopsis genome-sequencing programme, crown galls induced by Agrobacterium tumefaciens may become a model system to study plant tumour development. The molecular mechanisms of nutrient supply to support tumour growth and development are still unknown. In this study, we have identified a unique profile of Shaker-like potassium channels in agrobacteria-induced Arabidopsis tumours. Comparing the gene expression pattern of rapidly growing tumours with that of non-infected tissues, we found the suppression of shoot in favour of root-specific K+ channels. Among these, the upregulation of AKT1 and AtKC1 and the suppression of AKT2/3 and GORK were most pronounced. As a consequence, K+ uptake and accumulation were elevated in the tumour (163 mm) compared to control tissues (92 mm). Patch clamp studies on tumour protoplasts identified a population expressing the electrical properties of the AKT1 K+ channel. Furthermore, plants lacking a functional AKT1 or the AKT2/3 phloem K+ channel gene did not support tumour growth. This indicates that the delivery of potassium by AKT1 and the direction of assimilates, triggered by AKT2/3, are essential for tumour growth.

摘要

在拟南芥基因组测序计划完成后,根癌农杆菌诱导形成的冠瘿瘤可能成为研究植物肿瘤发育的模型系统。支持肿瘤生长和发育的营养供应分子机制仍不清楚。在本研究中,我们在农杆菌诱导的拟南芥肿瘤中鉴定出了一种独特的类Shaker钾通道特征。通过比较快速生长的肿瘤与未感染组织的基因表达模式,我们发现茎部相关基因表达受抑制,而根部特异性钾通道基因表达占优势。其中,AKT1和AtKC1上调,AKT2/3和GORK下调最为明显。结果,与对照组织(92 mM)相比,肿瘤中的钾吸收和积累增加(163 mM)。对肿瘤原生质体的膜片钳研究鉴定出了一群具有AKT1钾通道电学特性的细胞。此外,缺乏功能性AKT1或AKT2/3韧皮部钾通道基因的植物无法支持肿瘤生长。这表明AKT1介导的钾运输以及由AKT2/3触发的同化物运输方向对肿瘤生长至关重要。

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