Arabidopsis Glutamate Receptor Homolog AtGLR3.5 Modulates Cytosolic Ca…
doi : 10.1104/pp.114.251298
Dongdong Kong,Chuanli Ju, Aisha Parihar, So Kim, Daeshik Cho,June M. Kwak
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 glutamate receptor homolog AtGLR3.5 is predominantly expressed in germinating seeds and increases cytosolic Ca2+ concentration ([Ca2+]cyt) that counteracts the effect of abscisic acid (ABA) to promote germination. Repression of AtGLR3.5 impairs [Ca2+]cyt elevation, significantly delays germination, and enhances ABA sensitivity in seeds, whereas overexpression of AtGLR3.5 results in earlier germination and reduced seed sensitivity to ABA. Furthermore, we show that Ca2+ suppresses the expression of ABA 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 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.