月季钙依赖蛋白激酶RhCDPK26参与灰霉病抗性的分子机制研究

长期以来，灰霉病的防治都是花卉栽培、采后过程中的世界性难题，也是我国月季生产流通的重要限制因素，常常造成毁灭性损失。为了获得高抗灰霉的月季新品种，我们以‘金玛丽’和‘北京红’为亲本进行杂交，建立了包含261个后代的F1群体。我们进而对该群体进行抗病鉴定和基因分型，最终找到五个与灰霉抗性相关的分子标记，其中标记scaffold552812相关性最为显著。在正向遗传学的研究基础上，利用反向遗传学工具，对与scaffold552812标记紧密连锁的候选基因进行病毒诱导基因沉默，发现其中RhCDPK26基因直接参与月季灰霉抗性。本项目拟对RhCDPK26介导的灰霉抗性展开工作，研究其下游信号转导的过程和关键靶标蛋白，以期初步阐明RhCDPK26为代表的钙依赖蛋白激酶调节月季灰霉抗性信号的分子机制，进而为月季抗病品质改良提供新的思路和基因资源。

Gray mold caused by Botrytis cinerea is one of the most devastating diseases of rose in China, and worldwide as well. We employed an association mapping of 261 F1 roses crossed by ‘Goldmarie’ and ‘Beijinghong’. Among significant associations, a loci associated with resistance against B. cinerea was identified and predicted to encode a calcium-dependent protein kinase, namely RhCDPK26. Multiple lines of evidence, including transcriptomics, pathogen assay and virus induced gene silencing (VIGS), support the hypothesized function of this candidate gene RhCDPK26 in the rose response to B. cinerea. In this project, we aimed to investigate crucial role of RhCDPK26 in rose resistance against B. cinerea. This study will represent characterization of CDPKs involved in resistance to B. cinerea for the first time and provides new clues to elucidate rose disease response mechanism.