Figure 8.

The possible mechanisms by which Phe treatment represses the sscd1 cell death. The SSCD1 gene encodes FAH catalyzing the last step of Tyr degradation pathway. Disruption of FAH in sscd1 reduces Chl biosynthesis, which impairs the feedback inhibition of Chl biosynthesis from light–dark transition under SD, leading to the accumulation of ROS and then cell death (red lines and arrows). Phe treatment promotes Chl biosynthesis, which increases the feedback inhibition of Chl biosynthesis from light–dark transition under SD, reducing ROS and subsequent cell death (green arrows and lines). Meanwhile, Phe treatment activates phenylpropanoid pathway, which reduces ROS and subsequent cell death (blue arrows and lines). In the sscd1 mutant, ROS induces cell death and the JA production. JA up-regulates Tyr degradation pathway through COI1, promoting cell death, however, it also up-regulates PAL1 through COI1, which activates phenylpropanoid pathway, repressing cell death. The effect of MeJA treatment on sscd1 cell death through phenylpropanoid pathway might be greater than that through Tyr degradation pathway, resulting in that MeJA treatment enhances the repression of sscd1 cell death by Phe. Arrows indicate induction or positive regulation, whereas lines indicate repression or negative regulation. Arrows with dashed lines indicate multiple steps. FAH fumarylacetoacetate hydrolase; Chl chlorophyll; SD short day; ROS reactive oxygen species; Phe phenylalanine; JA jasmonates; MeJA methyl jasmonate; HGA homogentisate; FAA fumarylacetoacetate; FA fumarate; AA acetoacetate.