Patnaik Alena, Kumar Aman, Behera Anshuman, Mishra Gayatri, Dehery Subrat Kumar, Panigrahy Madhusmita, Das Anath Bandhu, Panigrahi Kishore C S
School of Biological Sciences, National Institute of Science Education and Research (NISER) Bhubaneswar, Jatni, Odisha, India.
Homi Bhabha National Institute (HBNI), Training School Complex, Anushakti Nagar, Mumbai, India.
Front Plant Sci. 2023 Mar 9;14:1091644. doi: 10.3389/fpls.2023.1091644. eCollection 2023.
GIGANTEA (GI) is a plant-specific nuclear protein that plays a pleiotropic role in the growth and development of plants. GI's involvement in circadian clock function, flowering time regulation, and various types of abiotic stress tolerance has been well documented in recent years. Here, the role of GI in response to () infection is investigated at the molecular level comparing Col-0 WT with the mutant in . Disease progression, photosynthetic parameters, and comparative anatomy confirmed that the spread and damage caused by pathogen infection were less severe in than in Col-0 WT plants. infection induces a remarkable accumulation of GI protein. Our report showed that it is not involved in flowering time regulation during infection. Estimation of defense hormone after infection showed that jasmonic acid (JA) level is higher and salicylic acid (SA) level is lower in compared to Col-0 WT. Here, we show that the relative transcript expression of () and () as a marker of the JA pathway is significantly higher while () and (), the markers of the SA pathway, are downregulated in the mutants compared to Col-0 plants. The present study convincingly suggests that the GI module promotes susceptibility to infection by inducing the SA pathway and inhibiting JA signaling in .
巨大蛋白(GI)是一种植物特有的核蛋白,在植物的生长发育中发挥着多效性作用。近年来,GI参与生物钟功能、开花时间调控以及各种非生物胁迫耐受性的作用已得到充分记录。在此,在分子水平上研究了GI在应对()感染时的作用,将Col-0野生型与()中的突变体进行比较。疾病进展、光合参数和比较解剖学证实,病原体感染在()中造成的传播和损害比在Col-0野生型植物中要轻。()感染诱导了GI蛋白的显著积累。我们的报告表明,它在()感染期间不参与开花时间调控。感染后防御激素的测定表明,与Col-0野生型相比,()中的茉莉酸(JA)水平较高,水杨酸(SA)水平较低。在此,我们表明,与Col-0植物相比,作为JA途径标志物的()和()的相对转录本表达在()突变体中显著更高,而SA途径的标志物()和()则下调。本研究令人信服地表明,GI模块通过在()中诱导SA途径并抑制JA信号传导来促进对()感染的易感性。