Waterlogging is one of the most serious abiotic stressors affecting Chrysanthemum morifolium during its lifespan. However, the molecular mechanisms underlying the waterlogging tolerance of chrysanthemum remain unclear. In this study, we discovered that the transcriptional coactivator MULTIPROTEIN BRIDGING FACTOR 1c (CmMBF1c) was significantly induced by waterlogging stress in chrysanthemums. Promoter sequence analysis and transient dual-luciferase assay using chrysanthemum protoplasts showed that the waterlogging-tolerant cultivar ‘Nannongxuefeng’ carried more response elements involved in waterlogging and hypoxia stress compared with the waterlogging-sensitive cultivar ‘Qinglu’, conferring ‘Nannongxuefeng’ a stronger hypoxia responsive activity and higher CmMBF1c expression under waterlogging conditions. Subcellular localization and transcriptional activity assays showed that CmMBF1c protein was localized to the nucleus and had no transcriptional activation activity. Overexpression of CmMBF1c in ‘Qinglu’ enhanced its waterlogging tolerance by promoting its ROS scavenging ability and maintaining low reactive oxygen species (ROS) levels. However, RNAi-mediated knockdown of CmMBF1c in cultivar ‘Nannongxuefeng’ resulted in the opposite tendency. Yeast two-hybrid screening and tobacco bimolecular fluorescence complementation (BiFC) assays revealed that CmHRE2, a pivotal regulator of hypoxia response, could interact with CmMBF1c. In summary, this study demonstrates that CmMBF1c improves chrysanthemum waterlogging tolerance by regulating its ROS signaling pathway and interacting with CmHRE2. These findings together offer, to our knowledge, new mechanistic insights into chrysanthemum waterlogging tolerance and provide a rational foundation for future research on the genetic improvement of horticultural crops for waterlogging stress tolerance.

中文翻译：

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菊花耐涝需要转录共激活因子 CmMBF1c

涝渍是影响菊花生命周期的最严重的非生物胁迫因素之一。然而，菊花耐涝性的分子机制仍不清楚。在这项研究中，我们发现转录共激活因子多蛋白桥接因子 1c (CmMBF1c) 被菊花的涝渍胁迫显着诱导。启动子序列分析和菊花原生质体瞬时双荧光素酶分析表明，与耐涝品种'青露'相比，耐涝品种'南农雪峰'携带更多的参与涝害和缺氧胁迫的响应元件，赋予'南农雪峰'更强的缺氧能力在涝渍条件下响应活性和更高的 CmMBF1c 表达。亚细胞定位和转录活性测定表明，CmMBF1c 蛋白定位于细胞核，没有转录激活活性。'青鹭'中 CmMBF1c 的过表达通过促进其 ROS 清除能力和维持低活性氧 (ROS) 水平来增强其耐涝性。然而，RNAi 介导的 CmMBF1c 在栽培品种'南农雪峰'中的敲低导致了相反的趋势。酵母双杂交筛选和烟草双分子荧光互补 (BiFC) 测定表明，缺氧反应的关键调节因子 CmHRE2 可以与 CmMBF1c 相互作用。总之，本研究表明 CmMBF1c 通过调节其 ROS 信号通路并与 CmHRE2 相互作用来提高菊花的耐涝性。据我们所知，这些发现共同提供，