Skip to main content
. Author manuscript; available in PMC: 2017 Dec 5.
Published in final edited form as: Dev Cell. 2016 Nov 23;39(5):597–610. doi: 10.1016/j.devcel.2016.10.020

Figure 7. Light induces EIN3 degradation via phyB to remove EIN3-maintained skotomorphogenesis for de-etiolation initiation.

Figure 7

(A and B) Images of seedling cotyledon phenotypes (A), and the angle of cotyledon opening (B). The seedlings were grown in the dark for 3 days and then maintained in the dark for 1 day (D4) or exposed to red light for 1 (D3R1) or 4 days (D3R4).

(C and D) Images of cotyledons (C) and the areas (D) of a single cotyledon. The seedlings were grown on 1/2 MS medium in the dark for 3 days and then exposed to red light for an additional 4 days (D3R4). Mean ± s.d., n>20.

(E) qRT-PCR results showing the expression of light-regulated EIN3 target genes in WT, EIN3ox, ein3eil1, EIN3ox/phyB, ein3eil1phyB and phyB. The seedlings were grown in the dark for 3 days and then subjected to additional red light exposure for 2 hr. Gene transcription was normalized to PP2A. Mean ±s.d., n=3.

(F) A working model depicting how phyB directly transduces the light signal to turn off EIN3-maintained skotomorphogenesis. Red light activates phyB, leading to its translocation from the cytoplasm to the nucleus, where phyB directly binds to both EIN3 and its E3 ligases EBF1/EBF2, enhancing the interactions of EBF1/EBF2 and EIN3 to rapidly degrade EIN3. As a result, light, acting through the photoreceptor, directly abolishes the action of EIN3, eliminating EIN3's repression on de-etiolation.