Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 119, Issue 34, Pages -Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2205920119
Keywords
calcium channel; CNGC15; DMI1; NF signaling; nuclear calcium spiking
Categories
Funding
- CAS Project for Young Scientists in Basic Research [YSBR-011]
- National Key R&D Program of China [2016YFA0500500]
- National Natural Science Foundation of China [32170243]
- Strategic Priority Research Program of the CAS [XDB27040208]
- Bill and Melinda Gates Foundation
- Foreign, Commonwealth and Development Office [OPP1028264]
- Bill and Melinda Gates Foundation [OPP1028264] Funding Source: Bill and Melinda Gates Foundation
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Nuclear Ca2+ oscillations play a crucial role in plant recognition of beneficial microsymbionts, and DMI1 and CNGC15 coordinate the oscillations. Gain-of-function mutations in DMI1 activate the channel complex, leading to spontaneous nuclear Ca2+ oscillations and nodulation. These mutations destabilize the hydrogen bond or salt-bridge network between RCK domains, resulting in structural changes and activation of the channel complex.
Nuclear Ca2+ oscillations allow symbiosis signaling, facilitating plant recognition of beneficial microsymbionts, nitrogen-fixing rhizobia, and nutrient-capturing arbuscular mycorrhizal fungi. Two classes of channels, DMI1 and CNGC15, in a complex on the nuclear membrane, coordinate symbiotic Ca2+ oscillations. However, the mechanism of Ca2+ signature generation is unknown. Here, we demonstrate spontaneous activation of this channel complex, through gain-of-function mutations in DMI1, leading to spontaneous nuclear Ca2+ oscillations and spontaneous nodulation, in a CNGC15-dependent manner. The mutations destabilize a hydrogen-bond or salt-bridge network between two RCK domains, with the resultant structural changes, alongside DMI1 cation permeability, activating the channel complex. This channel complex was reconstituted in human HEK293T cell lines, with the resultant calcium influx enhanced by autoactivated DMI1 and CNGC15s. Our results demonstrate the mode of activation of this nuclear channel complex, show that DMI1 and CNGC15 are sufficient to create oscillatory Ca2+ signals, and provide insights into its native mode of induction.
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