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Original Articles

Functional characterisation of MdMYB44 as a negative regulator in the response to cold and salt stress in apple calli

, , , &
Pages 347-355 | Accepted 17 Aug 2017, Published online: 13 Sep 2017
 

ABSTRACT

MYB (v-myb avian myeloblastosis viral oncogene homolog) transcription factors (TFs) participate in the abiotic stress response in several plant species. In this study, we cloned and characterised MdMYB44 from apple (Malus domestica). Phylogenetic analysis showed that the MdMYB44 protein was highly homologous to Arabidopsis thaliana MYB44. In addition, MdMYB44 localised to the nuclei in transformed onion epidermal cells and showed transcriptional activation activity in a yeast one-hybrid assay. MdMYB44 was expressed in the stem, leaves, roots, flowers, and fruits, with the highest transcript level being observed in the leaves. Quantitative PCR analysis demonstrated that MdMYB44 expression was down-regulated by cold, osmotic, and salt stresses. Furthermore, stable overexpression of MdMYB44 in transgenic apple calli remarkably alleviated their tolerance to high salinity and cold, and relative conductivity and malondialdehyde accumulation under salt and cold treatments were significantly higher than those in wild-type control calli. Therefore, our findings provide evidence that MdMYB44 is involved in susceptibility to cold and salt stress in apple calli and indicate MdMYB44 to negatively regulate plant abiotic stress defence.

Disclosure statement

No potential conflict of interest was reported by the authors.

Supplementary material

Supplemental data for this article can be accessed here.

Additional information

Funding

This work was supported by the Earmarked Fund for China Agriculture Research System (CARS-27), and science and technology support program (2014BAD16B03), and the Key Laboratory of Beijing Municipality of Stress Physiology and Molecular Biology for Fruit Trees, and the Beijing Collaborative Innovation Center for Eco-environmental Improvement with Forestry and Fruit Trees (CEFF-PXM2017-014207-000043).

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