《植物生理学报》 2014, 50(4): 501-509

过表达LeNLP4转录因子提高番茄抗低温胁迫能力

左衍秋, 马娜娜, 梁晓庆, 岳萌萌, 孟庆伟*

山东农业大学生命科学学院, 作物生物学国家重点实验室, 山东泰安271018

通信作者：孟庆伟；E-mail: qwmeng@sdau.edu.cn；Tel: 0538-8249606

摘　要：

NAC (NAM-ATAF1,2-CUC2)转录因子在植物胁迫响应中起重要作用。为了探讨LeNLP4基因在番茄抗低温胁迫中的功能, 分离了番茄LeNLP4转录因子基因, 并获得转正义LeNLP4基因番茄植株。荧光定量PCR分析表明, LeNLP4的表达受低温诱导。与野生型植株相比, 在4 ℃胁迫下转基因植株具有较高的生长量和光系统II (PSII)最大光化学效率(F_v/F_m)、过氧化氢(H₂O₂)和超氧阴离子(O₂.−)清除速率、抗坏血酸过氧化物酶(APX)和超氧化物歧化酶(SOD)活性, 以及较低的丙二醛(MDA)含量和相对电导率(REC)。过表达株系中SlCBF1的表达高于野生型。上述结果表明, LeNLP4的过表达提高了转基因番茄抗低温胁迫能力。

关键词：番茄; 低温胁迫; LeNLP4; SlCBF1; 活性氧

收稿：2013-11-21   修定：2014-03-20

资助：国家重点基础研究发展计划(2009CB118505)和国家自然科学基金(31171474和31371553)。

Overexpression of LeNLP4 Transcription Factor Improved the Chilling Tolerance of Tomato (Lycopersicon esculentum Mill.)

ZUO Yan-Qiu, MA Na-Na, LIANG Xiao-Qing, YUE Meng-Meng, MENG Qing-Wei*

State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai’an, Shandong 271018, China

Corresponding author: MENG Qing-Wei; E-mail: qwmeng@sdau.edu.cn; Tel: 0538-8249606

Abstract:

NAC (NAM-ATAF1,2-CUC2) family members play important roles in various environmental responses. In order to investigate the function of LeNLP4 under chilling stress, LeNLP4 was isolated from tomato (Lycopersicon esculentum) and transgenic plants were obtained. qRT-PCR confirmed that the expression of LeNLP4 was induced by chilling stress. Compared with the wild type (WT), transgenic tomato plants have higher growth increment and the maximal photochemistry efficiency of photosystem II (Fv/Fm), higher capability for scavenging hydrogen peroxide (H2O2) and superoxide radical (O2 .−), higher ascorbate peroxidase (APX) and superoxide dismutase (SOD), and lower malondialdehyde (MDA) content and the relative electric conductivity (REC) under chilling treatment. Expression level of SlCBF1 in transgenic lines was higher than that in WT. These results indicated that overexpression of LeNLP4 enhanced chilling tolerance of transgenic tomato plants.

Key words: tomato; chilling stress; LeNLP4; SlCBF1; reactive oxygen species