Responds to BcCBF2 and Induces Flavonol Biosynthesis to Enhance Tolerance under Cold Stress in Non-Heading Chinese Cabbage.

Int J Mol Sci

State Key Laboratory of Crop Genetics & Germplasm Enhancement and Utilization, Key Laboratory of Biology and Genetic Improvement of Horticultural Crops (East China), Engineering Research Center of Germplasm Enhancement and Utilization of Horticultural Crops, Nanjing Agricultural University, Nanjing 210095, China.

Published: May 2023

Flavonols have been shown to respond to a variety of abiotic stresses in plants, including cold stress. Higher total flavonoid content was found in non-heading Chinese cabbage (NHCC, (syn. ) ssp. ) after cold stress. A non-targeted metabolome analysis showed a significant increase in flavonol content, including that of quercetin and kaempferol. Here, we found that an R2R3-MYB transcription factor, , may play a role in this process. was up-regulated in response to cold treatment, with an accompanying accumulation of flavonols. Then, it was found that BcMYB111 could regulate the synthesis of flavonols by directly binding to the promoters of and . In the transgenic hairy roots of NHCC or stable transgenic , overexpression of increased flavonol synthesis and accumulation, while these were reduced in virus-induced gene silencing lines in NHCC. After cold stress, the higher proline content and lower malondialdehyde (MDA) content showed that there was less damage in transgenic than in the wild-type (WT). The transgenic lines performed better in terms of antioxidant capacity because of their lower HO content and higher superoxide dismutase (SOD) and peroxidase (POD) enzyme activities. In addition, a key cold signaling gene, BcCBF2, could specifically bind to the DRE element and activate the expression of in vitro and in vivo. The results suggested that played a positive role in enhancing the flavonol synthesis and cold tolerance of NHCC. Taken together, these findings reveal that cold stress induces the accumulation of flavonols to increase tolerance via the pathway of BcCBF2-BcMYB111-BcF3H/BcFLS1 in NHCC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10217907PMC
http://dx.doi.org/10.3390/ijms24108670DOI Listing

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