Modified expression of a heat shock protein gene, CaHSP22.0, results in high sensitivity to heat and salt stress in pepper (Capsicum annuum L.)

文献类型： 外文期刊

第一作者： Sun, Jian-Tian

作者： Sun, Jian-Tian;Cheng, Guo-Xin;Huang, Liu-Jun;Liu, Shuai;Ali, Muhammad;Khan, Abid;Gong, Zhen-Hui;Yu, Qing-Hui;Yang, Sheng-Bao;Luo, De-Xu

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关键词： Transgenic Arabidopsis; Gene silencing; Heat shock proteins; Capsicum annuum; Gene expression

期刊名称：SCIENTIA HORTICULTURAE （ 影响因子：3.463； 五年影响因子：3.672 ）

ISSN： 0304-4238

年卷期： 2019 年 249 卷

页码：

收录情况： SCI

摘要： Small heat shock proteins (sHSPs) are ubiquitous and diverse molecular chaperones. However, the contribution of sHSPs in pepper response to stress is controversial. In the study, we characterized a small heat shock protein gene CaHSP22.0 from pepper sHSP20s family, and found that the deduced amino acid sequence of CaHSP22.0 gene contained the conserved necessary domains and residue for sHSPs functions. Under normal condition, CaHSP22.0 was detected in all pepper organs, but its transcript level was up-regulated under high temperature and salt stress. CaHSP22.0-silenced pepper exhibits more sensitive to heat and salt stress, which was primarily reflected by aggravated chlorophyll degradation, increased leaf conductivity, level of superoxide anion free radical and malondialdehyde content. Interestingly, CaHSP22.0 overexpression also resulted in Arabidopsis sensitivity to high temperature and salt stress by inhibiting normal growth of leaves and roots, increasing superoxide anion free radical, decreasing activities of antioxidant enzymes and chlorophyll content, increasing malondialdehyde content, and disturbing low expression of genes involved in environment stress. Our results suggested that modified expression of CaHSP22.0 conferred peppers more sensitivity to high temperature and salt stress. The possible mechanism for CaHSP22.0 silencing is speculated to the damage to cell membrane; as for gene over-expression, the mechanism was complexed and might be the disruption of ROS caused by the improper levels of CaHSP22.0 with its substrates.

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