Melatonin confers cadmium tolerance by modulating critical heavy metal chelators and transporters in radish plants

Journal of Pineal Research - Tập 69 Số 1 - 2020
Liang Xu1, Fei Zhang1, Mingjia Tang1, Li Wang1, Junhui Dong1, Jiali Ying1, Yinglong Chen2, Bing Hu3, Cui Li1, Liwang Liu1
1National Key Laboratory of Crop Genetics and Germplasm Enhancement, Key Laboratory of Horticultural Crop Biology and Genetic Improvement (East China) of MOAR, College of Horticulture, Nanjing Agricultural University, Nanjing, China
2School of Agriculture and Environment The UWA’s Institute of Agriculture The University of Western Australia Perth WA Australia
3College of Life Science, Nanjing Agricultural University, Nanjing, China

Tóm tắt

Abstract

Cadmium (Cd) is an environmental pollutant that causes health hazard to living organisms. Melatonin (MT) has emerged as a ubiquitous pleiotropic molecule capable of coordinating heavy metal (HM) stresses in plants. However, it remains unclear how melatonin mediates Cd homeostasis and detoxification at transcriptional and/or post‐transcriptional levels in radish. Herein, the activities of five key antioxidant enzymes were increased, while root and shoot Cd contents were dramatically decreased by melatonin. A combined small RNA and transcriptome sequencing analysis showed that 14 differentially expressed microRNAs (DEMs) and 966 differentially expressed genes (DEGs) were shared between the Cd and Cd + MT conditions. In all, 23 and ten correlated miRNA‐DEG pairs were identified in Con vs. Cd and Con vs. Cd + MT comparisons, respectively. Several DEGs encoding yellow stripe 1‐like (YSL), heavy metal ATPases (HMA), and ATP‐binding cassette (ABC) transporters were involved in Cd transportation and sequestration in radish. Root exposure to Cd2+ induced several specific signaling molecules, which consequently trigger some HM chelators, transporters, and antioxidants to achieve reactive oxygen species (ROS) scavenging and detoxification and eliminate Cd toxicity in radish plants. Notably, transgenic analysis revealed that overexpression of the RsMT1 (Metallothionein 1) gene could enhance Cd tolerance of tobacco plants, indicating that the exogenous melatonin confers Cd tolerance, which might be attributable to melatonin‐mediated upregulation of RsMT1 gene in radish plants. These results could contribute to dissecting the molecular basis governing melatonin‐mediated Cd stress response in plants and pave the way for high‐efficient genetically engineering low‐Cd‐content cultivars in radish breeding programs.

Từ khóa


Tài liệu tham khảo

10.1016/j.tplants.2012.08.003

10.1039/c3mt00038a

10.1039/C8MT00247A

10.1016/j.scitotenv.2018.07.002

10.3389/fpls.2018.00012

10.3389/fpls.2015.01143

10.1007/s11103-013-0120-6

10.1016/j.plantsci.2017.05.001

10.1021/acs.jafc.7b01164

10.1104/pp.18.00485

10.1021/acs.jafc.9b02404

10.3390/molecules22101791

10.3390/molecules23020388

10.1016/j.jhazmat.2019.121727

10.1111/jpi.12526

10.3390/ijms20030709

10.1111/jpi.12253

10.1111/jpi.12359

10.3390/molecules23030584

10.3390/ijms20051040

10.3390/molecules23010165

10.3390/molecules24091826

10.1038/s41598-018-28561-0

10.1111/jpi.12346

10.1111/jpi.12392

10.1111/jpi.12387

10.3389/fpls.2015.00601

10.3390/molecules23040799

10.1007/s00122-012-1858-y

10.1093/jxb/ert240

10.1016/j.plantsci.2015.04.015

10.3390/molecules23020386

10.1007/s00122-016-2708-0

10.1038/nmeth.1923

10.1186/gb-2013-14-4-r36

10.1186/s13059-014-0550-8

10.1186/1471-2105-13-140

10.1093/nar/gkr688

10.1093/nar/gks554

10.1186/gb-2010-11-2-r14

10.1006/meth.2001.1262

10.1016/j.chemosphere.2019.03.026

10.3390/ijms13067828

10.3390/molecules23092352

10.1111/jpi.12232

10.3390/ijms19010316

10.1111/jpi.12167

10.1007/s00726-010-0809-7

10.7554/eLife.41124

10.1038/ncomms14033

10.1007/s00299-016-2079-7

10.1111/pce.12870

10.1111/pce.12747

10.1093/pcp/pcr166

10.1104/pp.113.216564

10.1016/j.molp.2016.02.003

10.1039/C8MT00374B

10.1093/pcp/pcx131

10.1111/pce.13471

10.1038/s41587-019-0038-x

10.1016/j.molp.2019.06.009

10.1038/s41438-020-0258-8

10.1038/s41598-017-14832-9

10.1016/j.molp.2018.05.005

10.1038/ncomms12617

10.1038/nbt.4273

10.1186/s13059-015-0826-7