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抗坏血酸盐通过调节脱落酸水平减轻棉花缺铁诱导的胁迫

Ascorbate Alleviates Fe Deficiency-Induced Stress in Cotton () by Modulating ABA Levels.

作者信息

Guo Kai, Tu Lili, Wang Pengcheng, Du Xueqiong, Ye Shue, Luo Ming, Zhang Xianlong

机构信息

National Key Laboratory of Crop Genetic Improvement, Huazhong Agricultural University Wuhan, China.

Key Laboratory of Biotechnology and Crop Quality Improvement of Ministry of Agriculture, Biotechnology Research Center, Southwest University Chongqing, China.

出版信息

Front Plant Sci. 2017 Jan 4;7:1997. doi: 10.3389/fpls.2016.01997. eCollection 2016.

Abstract

Fe deficiency causes significant losses to crop productivity and quality. To understand better the mechanisms of plant responses to Fe deficiency, we used an cotton ovule culture system. We found that Fe deficiency suppressed the development of ovules and fibers, and led to tissue browning. RNA-seq analysis showed that the -inositol and galacturonic acid pathways were activated and cytosolic () was suppressed in Fe-deficient treated fibers, which increased ASC (ascorbate) concentrations to prevent tissue browning. Suppression of cytosolic by RNAi in cotton increased ASC contents and delayed tissue browning by maintaining ferric reduction activity under Fe-deficient conditions. Meanwhile, RNAi line also exhibited the activation of expression of () and () to adapt to Fe deficiency. Abscisic acid (ABA) levels were significantly decreased in Fe-deficient treated ovules and fibers, while the upregulated expression of ABA biosynthesis genes and suppression of ABA degradation genes in Fe-deficient ovules slowed down the decreased of ABA in cytosolic suppressed lines to delay the tissue browning. Moreover, the application of ABA in Fe-deficient medium suppressed the development of tissue browning and completely restored the ferric reduction activity. In addition, ABA 8'-hydroxylase gene () overexpressed cotton has a decreased level of ABA and shows more sensitivity to Fe deficiency. Based on the results, we speculate that ASC could improve the tolerance to Fe deficiency through activating Fe uptake and maintaining ABA levels in cotton ovules and fibers, which in turn reduces symptom formation.

摘要

缺铁会导致作物生产力和品质大幅下降。为了更好地理解植物对缺铁反应的机制,我们使用了棉花胚珠培养系统。我们发现缺铁会抑制胚珠和纤维的发育,并导致组织褐变。RNA测序分析表明,缺铁处理的纤维中肌醇和半乳糖醛酸途径被激活,细胞质苹果酸脱氢酶(MDH)受到抑制,这增加了抗坏血酸(ASC)的浓度以防止组织褐变。通过RNA干扰抑制棉花中的细胞质MDH,在缺铁条件下通过维持铁还原活性增加了ASC含量并延缓了组织褐变。同时,RNA干扰株系还表现出铁吸收相关基因(IRT1)和黄化素还原酶基因(FRO2)表达的激活以适应缺铁。缺铁处理的胚珠和纤维中脱落酸(ABA)水平显著降低,而缺铁胚珠中ABA生物合成基因的上调表达和ABA降解基因的抑制减缓了细胞质MDH抑制株系中ABA的下降,从而延缓了组织褐变。此外,在缺铁培养基中施用ABA抑制了组织褐变的发展并完全恢复了铁还原活性。另外,ABA 8'-羟化酶基因(ABAH)过表达的棉花ABA水平降低,对缺铁表现出更高的敏感性。基于这些结果,我们推测ASC可以通过激活棉花胚珠和纤维中铁的吸收并维持ABA水平来提高对缺铁的耐受性,进而减少症状的形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8757/5209387/d069e432271e/fpls-07-01997-g001.jpg

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