■红蜘蛛螨(Tetranychusurticae)侵染(SMI)是室内种植的玫瑰的有害因素。尽管掠食性螨(Neoseiuluscalifornicus)拮抗作用(PMA)通常用于减轻SMI损伤,关于温室种植的玫瑰对SMI的防御反应以及PMA保护玫瑰的分子机制知之甚少。
■为了确定玫瑰对SMI和PMA的转录组和代谢组反应,玫瑰品种(“紫霞仙子/夜莺”)的叶子被荨麻疹感染,随后是捕食者螨的引入。在不同时间点收集叶样品并进行转录组和代谢组分析。
■我们发现SMI的24h在玫瑰叶片中对防御相关基因和代谢产物的表达产生了最大的变化。差异表达基因(DEG)和代谢物的KEGG途径分析显示,玫瑰对SMI和PMA的反应主要富集在倍半萜和三萜生物合成等途径中,苯并恶嗪类生物合成,二苯乙烯,二芳基庚酸和姜酚生物合成,植物甾醇生物合成,MAPK信号通路,苯丙素生物合成,和其他与抵抗生物应激相关的途径。玫瑰通过增加植物甾醇生物合成中结构基因和代谢物水平的表达与SMI和PMA反应,甲羟戊酸(MVA)途径,苯并恶嗪类生物合成,和二苯乙烯生物合成。此外,PMA导致SMI逐渐恢复,让玫瑰恢复到正常的生长状态。PMA恢复了SMI破坏的190个必需基因在玫瑰叶片中的表达,包括转录因子DRE1C,BH035、MYB14、EF110、WRKY24、NAC71和MY108。然而,PMA治疗144小时后,玫瑰对刺激的反应减弱,192小时后,有机酸和脂质的代谢水平在很大程度上得到了恢复。
■总而言之,我们的结果提供了有关玫瑰如何协调其转录组和代谢组以对SMI和PMA做出反应的见解,因此,玫瑰如何发光,T.荨麻,和加利福尼亚的N.互动。
UNASSIGNED: Red spider mite (Tetranychus urticae) infestation (SMI) is a detrimental factor for roses grown indoors. Although predatory mite (Neoseiulus californicus) antagonism (PMA) is often utilized to alleviate SMI damage, little is known about the defensive response of greenhouse-grown roses to SMI and the molecular mechanism by which PMA protects roses.
UNASSIGNED: To determine the transcriptome and metabolome responses of roses to SMI and PMA, the leaves of a rose cultivar (\"Fairy Zixia/Nightingale\") were infested with T. urticae, followed by the introduction of predator mite. Leaf samples were collected at various time points and subjected to transcriptome and metabolome analyses.
UNASSIGNED: We found that 24 h of SMI exerted the most changes in the expression of defense-related genes and metabolites in rose leaves. KEGG pathway analysis of differentially expressed genes (DEGs) and metabolites revealed that rose responses to SMI and PMA were primarily enriched in pathways such as sesquiterpenoid and triterpenoid biosynthesis, benzoxazinoid biosynthesis, stilbenoid, diarylheptanoid and gingerol biosynthesis, phytosterol biosynthesis, MAPK signaling pathway, phenylpropanoid biosynthesis, and other pathways associated with resistance to biotic stress. Rose reacted to SMI and PMA by increasing the expression of structural genes and metabolite levels in phytosterol biosynthesis, mevalonate (MVA) pathway, benzoxazinoid biosynthesis, and stilbenoid biosynthesis. In addition, PMA caused a progressive recover from SMI, allowing rose to revert to its normal growth state. PMA restored the expression of 190 essential genes damaged by SMI in rose leaves, including transcription factors DRE1C, BH035, MYB14, EF110, WRKY24, NAC71, and MY108. However, after 144 h of PMA treatment, rose responsiveness to stimulation was diminished, and after 192 h, the metabolic levels of organic acids and lipids were recovered in large measure.
UNASSIGNED: In conclusion, our results offered insights on how roses coordinate their transcriptome and metabolome to react to SMI and PMA, therefore shedding light on how roses, T. urticae, and N. californicus interact.