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褪黑素相关基因的异源表达提高了. 的耐盐性。

Heterologous Expression of the Melatonin-Related Gene Improves Salt Tolerance in .

机构信息

State Key Laboratory of Crop Stress Biology for Arid Areas/Shaanxi Key Laboratory of Apple, College of Horticulture, Northwest A & F University, Yangling, Xianyang 712100, China.

出版信息

Int J Mol Sci. 2021 Nov 17;22(22):12425. doi: 10.3390/ijms222212425.

DOI:10.3390/ijms222212425
PMID:34830307
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8620682/
Abstract

Melatonin, a widely known indoleamine molecule that mediates various animal and plant physiological processes, is formed from N-acetyl serotonin via N-acetylserotonin methyltransferase (ASMT). ASMT is an enzyme that catalyzes melatonin synthesis in plants in the rate-determining step and is homologous to hydroxyindole-O-methyltransferase (HIOMT) melatonin synthase in animals. To date, little is known about the effect of on salinity in apple plants. Here, we explored the melatonin physiological function in the salinity condition response by heterologous expressing the homologous human gene in apple plants. We discovered that the expression of melatonin-related gene () in apple plants was induced by salinity. Most notably, compared with the wild type, three transgenic lines indicated higher melatonin levels, and the heterologous expression of enhanced the expression of melatonin synthesis genes. The transgenic lines showed reduced salt damage symptoms, lower relative electrolyte leakage, and less total chlorophyll loss from leaves under salt stress. Meanwhile, through enhanced activity of antioxidant enzymes, transgenic lines decreased the reactive oxygen species accumulation, downregulated the expression of the abscisic acid synthesis gene (), accordingly reducing the accumulation of abscisic acid under salt stress. Both mechanisms regulated morphological changes in the stomata synergistically, thereby mitigating damage to the plants' photosynthetic ability. In addition, transgenic plants also effectively stabilized their ion balance, raised the expression of salt stress-related genes, as well as alleviated osmotic stress through changes in amino acid metabolism. In summary, heterologous expression of improved the adaptation of apple leaves to salt stress, primarily by increasing melatonin concentration, maintaining a high photosynthetic capacity, reducing reactive oxygen species accumulation, and maintaining normal ion homeostasis.

摘要

褪黑素是一种广泛存在的吲哚胺分子,它介导着各种动植物的生理过程,是通过 N-乙酰血清素甲基转移酶(ASMT)从 N-乙酰血清素合成的。ASMT 是一种在植物中催化褪黑素合成的限速酶,与动物中的羟基吲哚-O-甲基转移酶(HIOMT)褪黑素合酶同源。迄今为止,人们对褪黑素在苹果植物耐盐性中的作用知之甚少。在这里,我们通过在苹果植物中异源表达同源的人 ASMT 基因,探索了褪黑素在盐胁迫响应中的生理功能。我们发现,褪黑素相关基因()在苹果植物中受到盐胁迫的诱导。值得注意的是,与野生型相比,三个转基因株系表现出更高的褪黑素水平,并且异源表达 增强了褪黑素合成基因的表达。在盐胁迫下,转基因株系表现出较少的盐害症状、较低的相对电解质渗透率和较少的总叶绿素损失。同时,通过增强抗氧化酶的活性,转基因株系降低了活性氧的积累,下调了脱落酸合成基因()的表达,从而减少了盐胁迫下脱落酸的积累。这两种机制协同调节气孔形态变化,从而减轻对植物光合作用能力的损害。此外,转基因植物还通过改变氨基酸代谢有效地稳定了它们的离子平衡,提高了与盐胁迫相关的基因的表达,并缓解了渗透胁迫。总之,异源表达 提高了苹果叶片对盐胁迫的适应能力,主要是通过增加褪黑素浓度、维持高的光合作用能力、减少活性氧的积累和维持正常的离子平衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/20f4d3e99b53/ijms-22-12425-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/d0422f9c70c9/ijms-22-12425-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/0ddc18c94793/ijms-22-12425-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/d867a897bc07/ijms-22-12425-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/b3aa9272d059/ijms-22-12425-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/09e7c8e368e7/ijms-22-12425-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/8ce45996e7c5/ijms-22-12425-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/92776b8fc3a9/ijms-22-12425-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/7f80e74f7ad8/ijms-22-12425-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/20f4d3e99b53/ijms-22-12425-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/d0422f9c70c9/ijms-22-12425-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/0ddc18c94793/ijms-22-12425-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/d867a897bc07/ijms-22-12425-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/b3aa9272d059/ijms-22-12425-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/09e7c8e368e7/ijms-22-12425-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/8ce45996e7c5/ijms-22-12425-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/92776b8fc3a9/ijms-22-12425-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/7f80e74f7ad8/ijms-22-12425-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc4c/8620682/20f4d3e99b53/ijms-22-12425-g009.jpg

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