4.8 Article

An HD-ZIP transcription factor, MxHB13, integrates auxin-regulated and juvenility-determined control of adventitious rooting in Malus xiaojinensis

期刊

PLANT JOURNAL
卷 107, 期 6, 页码 1663-1680

出版社

WILEY
DOI: 10.1111/tpj.15406

关键词

adventitious root; auxin; Malus xiaojinensis; SPL26; HB13

资金

  1. National Natural Science Foundation of China [31672107, 31872053, 31801824]

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The research found that exogenous indole butyric acid treatment led to the downregulation of many genes in adult phase leafy cuttings of Malus xiaojinensis, including those involved in phytohormone signaling, carbohydrate metabolism, and cell dedifferentiation. By regulating the interaction between the MxHB13 gene and other regulatory factors, a model for AR formation in adult phase Malus xiaojinensis was proposed.
Adventitious root (AR) formation is a critical factor in the vegetative propagation of forestry and horticultural plants. Competence for AR formation declines in many species during the miR156/SPL-mediated vegetative phase change. Auxin also plays a regulatory role in AR formation. In apple rootstock, both high miR156 expression and exogenous auxin application are prerequisites for AR formation. However, the mechanism by which the miR156/SPL module interacts with auxin in controlling AR formation is unclear. In this paper, leafy cuttings of juvenile (Mx-J) and adult (Mx-A) phase Malus xiaojinensis were used in an RNA-sequencing experiment. The results revealed that numerous genes involved in phytohormone signaling, carbohydrate metabolism, cell dedifferentiation, and reactivation were downregulated in Mx-A cuttings in response to indole butyric acid treatment. Among the differentially expressed genes, an HD-ZIP transcription factor gene, MxHB13, was found to be under negative regulation of MdSPL26 by directly binding to MxHB13 promoter. MxTIFY9 interacts with MxSPL26 and may play a role in co-repressing the expression of MxHB13. The expression of MxTIFY9 was induced by exogenous indole butyric acid. MxHB13 binds to the promoter of MxABCB19-2 and positively affects the expression. A model is proposed in which MxHB13 links juvenility-limited and auxin-limited AR recalcitrance mechanisms in Mx-A.

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