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Mechanism of exogenous cytokinins inducing bulbil formation in Lilium lancifolium in vitro

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The cytokinin pathway promotes the initiation of bulbil formation, and iPA may an important type of cytokinin during bulbil formation in Lilium lancifolium.

Abstract

Bulbils are important vegetative reproductive organs in triploid Lilium lancifolium. We previously showed that cytokinins are involved in bulbil formation, but how cytokinins participate in bulbil formation is not clear. In this study, bulbil formation was divided into three stages on the basis of anatomical and histological observations: the bulbil initiation stage, bulbil primordium-formation stage and bulbil structure-formation stage. The results indicated that iPA was the most critical cytokinin during the bulbil initiation. qRT-PCR revealed that increased iPA content during bulbil initiation was mainly due to increased expression of cytokinin synthesis genes (IPT1/5) and cytokinin activation genes (LOG1/3/5/7) and significantly decreased expression of the cytokinin degradation gene CKX4. Exogenous 6-BA and lovastatin affected the cytokinin pathway and promoted or inhibited bulbil initiation by increasing or decreasing the content of endogenous iPA, respectively. In summary, we demonstrate that cytokinins positively regulate bulbil formation and provide preliminary insight into the regulatory mechanisms by which the cytokinin pathway promotes bulbil initiation.

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Acknowledgements

This study was supported by the National Natural Science Foundation of China (31902043, 31672196), National Key R&D Program of China (2019YFD1001002). This research was conducted at the Key Laboratory of Biology and Genetic Improvement of Horticultural Crops, Ministry of Agriculture, China.

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Correspondence to Jun Ming.

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Communicated by Xian Sheng Zhang.

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He, G., Yang, P., Tang, Y. et al. Mechanism of exogenous cytokinins inducing bulbil formation in Lilium lancifolium in vitro. Plant Cell Rep 39, 861–872 (2020). https://doi.org/10.1007/s00299-020-02535-x

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  • DOI: https://doi.org/10.1007/s00299-020-02535-x

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