Zou Kunkun, Li Yang, Zhang Wenjie, Jia Yunfeng, Wang Yang, Ma Yuting, Lv Xiangling, Xuan Yuanhu, Du Wanli
College of Agronomy, Shenyang Agricultural University, Shenyang, China.
College of Agronomy, Heilongjiang Bayi Agricultural University, Daqing, China.
Front Plant Sci. 2022 Sep 9;13:970897. doi: 10.3389/fpls.2022.970897. eCollection 2022.
Common smut, caused by (DC.) Corda, is a destructive fungal disease of maize worldwide; it forms large tumors, reducing corn yield and quality. However, the molecular defense mechanism to common smut in maize remains unclear. The present study aimed to use a leading maize inbred line Ye478 to analyze the response to inoculation. The histological and cytological analyses demonstrated that grew gradually to the host cells 6 h post-inoculation (hpi). The samples collected at 0, 3, 6, and 12 hpi were analyzed to assess the maize transcriptomic changes in response to . The results revealed differences in hormone signaling, glycometabolism, and photosynthesis after infection; specific changes were detected in jasmonic acid (JA), salicylic acid (SA), ethylene (ET), and abscisic acid (ABA) signaling pathways, glycolysis/gluconeogenesis, and photosystems I and II, probably related to defense response. MapMan analysis demonstrated that the differentially expressed genes between the treatment and control groups were clustered into light reaction and photorespiration pathways. In addition, inoculation induced chloroplast swelling and damage, suggesting a significant effect on the chloroplast activity and subsequent metabolic process, especially hexose metabolism. A further genetic study using wild-type and galactinol-sucrose galactosyltransferase () and yellow-green leaf-1 () mutants identified that these two -induced genes negatively regulated defense against common smut in maize. Our measurements showed the pathogen early-invasion process, and the key pathways of both chlorophyll biosynthesis and sugar transportation were critical modified in the infected maize line, thereby throwing a light on the molecular mechanisms in the maize- interaction.
由(DC.)科尔达引起的玉米丝黑穗病是一种在全球范围内对玉米具有毁灭性的真菌病害;它会形成大的肿瘤,降低玉米产量和品质。然而,玉米对玉米丝黑穗病的分子防御机制仍不清楚。本研究旨在利用优良玉米自交系掖478分析其对接种的反应。组织学和细胞学分析表明,接种后6小时(hpi)病菌逐渐向宿主细胞生长。对在0、3、6和12 hpi采集的样本进行分析,以评估玉米转录组对病菌接种的变化。结果显示,病菌感染后激素信号传导、糖代谢和光合作用存在差异;在茉莉酸(JA)、水杨酸(SA)、乙烯(ET)和脱落酸(ABA)信号通路、糖酵解/糖异生以及光系统I和II中检测到特定变化,可能与防御反应有关。MapMan分析表明,处理组和对照组之间的差异表达基因聚集在光反应和光呼吸途径中。此外,病菌接种导致叶绿体肿胀和损伤,表明对叶绿体活性及随后的代谢过程有显著影响,尤其是己糖代谢。使用野生型以及棉子糖 - 蔗糖半乳糖基转移酶()和黄绿叶片 - 1()突变体进行的进一步遗传研究确定,这两个病菌诱导基因对玉米抗玉米丝黑穗病防御起负调控作用。我们的测量结果显示了病原菌的早期入侵过程,并且在受感染的玉米品系中,叶绿素生物合成和糖运输的关键途径均发生了关键改变,从而揭示了玉米与病菌互作的分子机制。