bioRxiv · 10.1101/2024.08.29.610327
Integrated Dual-Channel Retrograde Signaling Directs Stress Responses by Degrading the HAT1/TPL/IMPalpha-9 Suppressor Complex and Activating CAMTA3
Abstract
The intricate communication between plastids and the nucleus, shaping stress-responsive gene expression, has long intrigued researchers. This study combines genetics, biochemical analysis, cellular biology, and protein modeling to uncover how the plastidial metabolite MEcPP activates the stress-response regulatory hub known as the Rapid Stress Response Element (RSRE). Specifically, we identify the HAT1/TPL/IMP- 9 suppressor complex, where HAT1 directly binds to RSRE and its activator, CAMTA3, masking RSRE and sequestering the activator. Stress-induced MEcPP disrupts this complex, exposing RSRE and releasing CAMTA3, while enhancing Ca2+ influx and raising nuclear Ca2+levels crucial for CAMTA3 activation and the initiation of RSRE- containing gene transcription. This coordinated breakdown of the suppressor complex and activation of the activator highlights the dual-channel role of MEcPP in plastid-to- nucleus signaling. It further signifies how this metabolite transcends its expected biochemical role, emerging as a crucial initiator of harmonious signaling cascades essential for maintaining cellular homeostasis under stress. SummaryThis study uncovers how the stress-induced signaling metabolite MEcPP disrupts the HAT1/TPL/IMP-9 suppressor complex, liberating the activator CAMTA3 and enabling Ca2+ influx essential for CAMTA3 activation, thus orchestrating stress responses via repressor degradation and activator induction.
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Zeng, L., Guo, J., Palayam, M., Rodriguez, C., Gomez Mendez, M. F., Wang, Y., Ven, W. v. d., Pruneda-Paz, J., Shabek, N., Dehesh, K.. 2024-08-30. Integrated Dual-Channel Retrograde Signaling Directs Stress Responses by Degrading the HAT1/TPL/IMPalpha-9 Suppressor Complex and Activating CAMTA3. https://doi.org/10.1101/2024.08.29.610327
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