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AtWNK8基因的破坏通过调节脯氨酸含量以及过氧化氢酶和过氧化物酶的活性,增强了拟南芥对盐胁迫和渗透胁迫的耐受性。

Disruption of AtWNK8 enhances tolerance of Arabidopsis to salt and osmotic stresses via modulating proline content and activities of catalase and peroxidase.

作者信息

Zhang Baige, Liu Kaidong, Zheng Yan, Wang Yingxiang, Wang Jinxiang, Liao Hong

机构信息

State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, Root Biology Center, College of Natural Resources and Environment, South China Agricultural University, Guangzhou 510642, China.

出版信息

Int J Mol Sci. 2013 Mar 27;14(4):7032-47. doi: 10.3390/ijms14047032.

Abstract

With no lysine kinases (WNKs) play important roles in plant growth and development. However, its role in salt and osmotic stress tolerance is unclear. Here, we report that AtWNK8 is mainly expressed in primary root, hypocotyl, stamen and pistil and is induced by NaCl and sorbitol treatment. Compared to the wild-type, the T-DNA knock-out wnk8 mutant was more tolerant to severe salinity and osmotic stresses, as indicated by 27% and 198% more fresh weight in the NaCl and sorbitol treatment, respectively. The wnk8 mutant also accumulated 1.43-fold more proline than the wild-type in the sorbitol treatment. Under NaCl and sorbitol stresses, catalase (CAT) activity in wnk8 mutant was 1.92- and 3.7-times of that in Col-0, respectively. Similarly, under salt and osmotic stress conditions, peroxidase (POD) activities in wnk8 mutant were 1.81- and 1.58-times of that in Col-0, respectively. Taken together, we revealed that maintaining higher CAT and POD activities might be one of the reasons that the disruption of AtWNK8 enhances the tolerance to salt stress, and accumulating more proline and higher activities of CAT and POD might result in the higher tolerance of WNK8 to osmotic stress.

摘要

无赖氨酸激酶(WNKs)在植物生长发育中发挥重要作用。然而,其在耐盐和渗透胁迫方面的作用尚不清楚。在此,我们报道AtWNK8主要在主根、下胚轴、雄蕊和雌蕊中表达,并受NaCl和山梨醇处理诱导。与野生型相比,T-DNA敲除wnk8突变体对严重盐度和渗透胁迫更具耐受性,在NaCl和山梨醇处理中鲜重分别增加27%和198%。在山梨醇处理中,wnk8突变体积累的脯氨酸也比野生型多1.43倍。在NaCl和山梨醇胁迫下,wnk8突变体中的过氧化氢酶(CAT)活性分别是Col-0中的1.92倍和3.7倍。同样,在盐胁迫和渗透胁迫条件下,wnk8突变体中的过氧化物酶(POD)活性分别是Col-0中的1.81倍和1.58倍。综上所述,我们揭示了维持较高的CAT和POD活性可能是AtWNK8缺失增强耐盐性的原因之一,而积累更多脯氨酸以及更高的CAT和POD活性可能导致wnk8对渗透胁迫具有更高的耐受性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76fc/3645675/0441df46acab/ijms-14-07032f1.jpg

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