Hans Barbora, Balažová Ema, Dokupilová Svetlana, Mikuš Peter, Balažová Andrea, Kubíková Renáta, Obložinský Marek
Department of Cell and Molecular Biology of Drugs, Faculty of Pharmacy, Comenius University Bratislava, Kalinčiakova 8, 832 32 Bratislava, Slovakia.
Department of Pharmaceutical Analysis and Nuclear Pharmacy, Faculty of Pharmacy, Comenius University Bratislava, Odbojárov 10, 832 32 Bratislava, Slovakia.
Plants (Basel). 2025 May 8;14(10):1413. doi: 10.3390/plants14101413.
Wounding triggers complex secondary metabolic pathways in plants, including benzylisoquinoline alkaloid (BIA) biosynthesis in opium poppy ( L.). This study explores transcriptional and metabolic responses to wounding and methyl jasmonate (MeJA) treatment, focusing on BIA biosynthesis and regulatory mechanisms. Real-time expression analysis revealed significant up-regulation of transcripts in the ()-reticuline and papaverine biosynthetic pathway, while the noscapine pathway was suppressed. The morphinan pathway also showed transcriptional activation, except in the case of codeinone reductase (), which remained unresponsive to both wounding and MeJA, suggesting a partially uncoupled mechanism. Metabolite profiling using HPLC-MS demonstrated a rapid accumulation of morphine post wounding, further supporting the hypothesis of independent regulatory control over . The role of phospholipase C (PLC) in modulating wound-induced BIA accumulation was investigated, revealing that PLC inhibition reduced morphine production and suppressed expression. These findings highlight the importance of phospholipid-dependent signalling in activating morphine biosynthesis, potentially at the expense of other BIAs. This study provides insights into plant stress responses and suggests strategies for enhancing BIA production through targeted interventions, offering potential applications in improving alkaloid yield.
创伤会触发植物体内复杂的次生代谢途径，包括罂粟（Papaver somniferum L.）中苄基异喹啉生物碱（BIA）的生物合成。本研究探讨了对创伤和茉莉酸甲酯（MeJA）处理的转录和代谢反应，重点关注BIA生物合成及其调控机制。实时表达分析显示，（-）-网状番荔枝碱和罂粟碱生物合成途径中的转录本显著上调，而那可丁途径受到抑制。吗啡喃途径也表现出转录激活，除了可待因酮还原酶（codeinone reductase），它对创伤和MeJA均无反应，这表明存在部分解偶联机制。使用HPLC-MS进行的代谢物谱分析表明，创伤后吗啡迅速积累，进一步支持了对吗啡独立调控的假设。研究了磷脂酶C（PLC）在调节创伤诱导的BIA积累中的作用，发现抑制PLC会降低吗啡产量并抑制相关基因表达。这些发现突出了磷脂依赖性信号传导在激活吗啡生物合成中的重要性，这可能是以牺牲其他BIA为代价的。本研究为植物应激反应提供了见解，并提出了通过靶向干预提高BIA产量的策略，为提高生物碱产量提供了潜在应用。
