Journal of Integrative Agriculture

• •    下一篇

PpMYB114促进梨花青苷的合成部分依赖于PpMYB10

  

  • 修回日期:2024-12-31

PpMYB114 partially depends on PpMYB10 for the promotion of anthocyanin accumulation in pear

Jiage Li1, 2, 3, 4, Rongling Qin1, 2, 3, 4, Yongchen Fang1, 3, 4, Yuhao Gao1, 3, 4, Yang Jiao1, 3, 4, Jia Wei1, 3, 4, Songling Bai1, 3, 4, Junbei Ni1, 2, 3, 4#, Yuanwen Teng1, 2, 3, 4#   

  1. 1 College of Agriculture and Biotechnology, Zhejiang University, Hangzhou, Zhejiang 310058, China

    2 Hainan Institute of Zhejiang University, Sanya, Hainan 572000, China

    3 Zhejiang Key Laboratory of Horticultural Crop Quality Improvement, Hangzhou 310058, Zhejiang, China

    4 The Key Laboratory of Horticultural Plant Growth, Development and Quality Improvement, Ministry of Agriculture of China, Hangzhou 310058, Zhejiang, China

  • Revised:2024-12-31
  • About author: #Correspondence Junbei Ni, E-mail: nijunbei@zju.edu.cn; Yuanwen Teng, E-mail: ywteng@zju.edu.cn
  • Supported by:

    The work was supported by the National Natural Science Foundation of China

    (32072545 and 32272678), the Young Elite Scientists Sponsorship Program by CAST (2023QNRC001), and the Zhejiang Provincial Natural Science Foundation of China (LY22C150003). 

摘要:

红(皮)梨的形成主要源于果皮中花青苷的积累,PpMYB10PpMYB114是正调控梨果皮花青苷合成的关键R2R3-MYB转录因子。我们前期研究发现乙烯通过抑制PpMYB10PpMYB114的表达抑制红梨花青苷合成,且PpERF9-PpTPL1共抑制复合体介导乙烯通过组蛋白去乙酰化作用抑制PpMYB114的表达,但PpMYB10的表达不受该复合体直接调控。因此,乙烯抑制PpMYB10表达的分子机制尚未阐明。本研究发现响应乙烯信号的条件下,PpMYB114PpMYB10 的表达模式高度相关。进一步研究表明PpMYB114通过直接结合PpMYB10 启动子区域上的MBSMYB结合位点)元件促进其表达。在成熟梨果实中瞬时过表达PpMYB114显著促进了PpMYB10的表达瞬时沉默PpMYB114则显著抑制了PpMYB10的表达。进一步,我们发现茄梨愈伤组织中过表达PpMYB114显著诱导了PpMYB10的表达和花青苷合成而在PpMYB114-OX愈伤组织中瞬时沉默PpMYB10则显著减弱了PpMYB114促进花青苷生物合成的作用,表明PpMYB114诱导梨花青苷合成至少部分依赖于转录激活PpMYB10。综上所述,以上结果表明乙烯可能通过抑制PpMYB114的表达进而抑制PpMYB10的表达。我们的研究结果为乙烯抑制PpMYB10表达的潜在机制提供了新的见解,并揭示了参与花青苷生物合成的R2R3-MYB转录因子之间的调控关系。

Abstract:

PpMYB10 and PpMYB114 have been identified as the key R2R3-MYB transcription factors (TFs) that positively regulate anthocyanin biosynthesis in pear. Our previous study demonstrated that the ethylene-induced PpERF9-PpTPL1 co-repressor complex represses PpMYB114 expression, but not PpMYB10, via histone deacetylation. However, the precise molecular mechanism underlying the ethylene-mediated inhibition of PpMYB10 expression remains to be elucidated. The results of the present study reveal a high correlation between the expression patterns of PpMYB114 and PpMYB10 in response to ethylene signaling. Moreover, PpMYB114 was found to promote the expression of PpMYB10 by directly binding to the MYB-bind site (MBS) element within its promoter region. Transient overexpression or silencing of PpMYB114 resulted in the promotion or inhibition of PpMYB10 expression in mature pear fruit, respectively. The overexpression of PpMYB114 in pear calli significantly induced PpMYB10 expression and anthocyanin biosynthesis. Conversely, transient silencing of PpMYB10 in PpMYB114-OX pear calli hindered the promotive effect of PpMYB114 on anthocyanin biosynthesis, indicating that PpMYB114 induces anthocyanin biosynthesis at least partially, depending on the transcriptionally activating PpMYB10. Collectively, these results indicate that ethylene may inhibit the expression of PpMYB10 by repressing PpMYB114. Our findings provide insights into a possible mechanism involving ethylene-inhibited PpMYB10 in pear and reveal the regulatory relationship between the R2R3-MYBs involved in anthocyanin biosynthesis. 

Key words: pear , PpMYB114 ,  , PpMYB10 ,  , transcriptional regulation ,  , anthocyanin