Arabidopsis Glutamate Receptor Homolog3.5 Modulates Cytosolic Ca²⁺ Level to Counteract Effect of Abscisic Acid in Seed Germination

• Published in: Plant physiology (Bethesda) 2015-04, Vol.167 (4), p.1630-1642
• Main Authors: Kong, Dongdong, Ju, Chuanli, Parihar, Aisha, Kim, So, Cho, Daeshik, Kwak, June M.
• Format: Article
• Language: English
• Subjects: Abscisic Acid - metabolism; Arabidopsis - genetics; Arabidopsis - physiology; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Biology; Calcium; Calcium - metabolism; Cytosol - metabolism; Embryos; Gene expression regulation; Gene Expression Regulation, Plant; Genes, Reporter; Germination; Glutamate receptors; Models, Biological; Mutation; Plant cells; Plant Growth Regulators - metabolism; Plants; Receptors, Glutamate - genetics; Receptors, Glutamate - metabolism; Seed germination; Seedlings; Seeds - genetics; Seeds - physiology; Signal Transduction; SIGNALING AND RESPONSE; Transcription Factors - genetics; Transcription Factors - metabolism
• ISSN: 0032-0889; 1532-2548; 1532-2548
• DOI: 10.1104/pp.114.251298

Seed germination is a critical step in a plant's life cycle that allows successful propagation and is therefore strictly controlled by endogenous and environmental signals. However, the molecular mechanisms underlying germination control remain elusive. Here, we report that the Arabidopsis (Arabidopsis thaliana) glutamate receptor homolog3.5 (AtGLR3.5) is predominantly expressed in germinating seeds and increases cytosolic Ca²⁺ concentration that counteracts the effect of abscisic acid (ABA) to promote germination. Repression ofAtGLR3.5impairs cytosolic Ca²⁺ concentration elevation, significantly delays germination, and enhances ABA sensitivity in seeds, whereas overexpression ofAtGLR3.5results in earlier germination and reduced seed sensitivity to ABA. Furthermore, we show that Ca²⁺ suppresses the expression ofABSCISIC ACID INSENSITIVE4(ABI4), a key transcription factor involved in ABA response in seeds, and that ABI4 plays a fundamental role in modulation of Ca²⁺-dependent germination. Taken together, our results provide molecular genetic evidence that AtGLR3.5-mediated Ca²⁺ influx stimulates seed germination by antagonizing the inhibitory effects of ABA through suppression of ABI4. These findings establish, to our knowledge, a new and pivotal role of the plant glutamate receptor homolog and Ca²⁺ signaling in germination control and uncover the orchestrated modulation of the AtGLR3.5-mediated Ca²⁺ signal and ABA signaling via ABI4 to fine-tune the crucial developmental process, germination, in Arabidopsis.