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. 2023 Jan 23;14:365. doi: 10.1038/s41467-023-35975-6

Fig. 7. Model for ethylene-induced CTR1 nuclear translocation and stimulation of the ethylene response.

Fig. 7

In the absence of ethylene, the ethylene receptors, CTR1, and EIN2 mainly localize to the ER. Receptor-activated CTR1 phosphorylates EIN2, thus leading to the proteolytic degradation of EIN2 via EIN2-TARGETING PROTEIN 1 (ETP1) and ETP2. In the presence of ethylene, the receptors, and hence CTR1, are inactivated. Inactivated CTR1 no longer phosphorylates EIN2, and the C-terminal domain of EIN2 (EIN2-CEND) is proteolytically cleaved and translocates to the nucleus, where it initiates the primary ethylene response via EIN3 activation. EIN2-CEND is also targeted to processing bodies (P-bodies) and suppresses EBF mRNA translation. After the nuclear translocation of EIN2-CEND, CTR1 is released from the receptors and relocates to the nucleus via an unknown mechanism. The nuclear-localized CTR1 directly interacts with EBF2, thus stabilizing EIN3 via an unknown mechanism and ultimately stimulating the ethylene response. The yellow square with a question mark indicates an unknown cargo protein that delivers CTR1 to the nucleus. Arrows indicate the movement of ethylene signaling components or positive influence; blunted ends indicate inhibition.