Supplementary data from: Bimodal retrograde signaling disrupts a suppressor network and activates a key transcriptional activator to direct stress responses

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/IMPα-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.