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The maize protein Rp1-D21, an autoactive derivative of the Rp1-D nucleotide-binding leucine rich repeat (NLR) disease resistance protein, triggers a spontaneous hypersensitive cell death defense response (HR). ZmCER9, a member of a class of E3 ligases involved in the endoplasmic reticulum associated degradation (ERAD) protein quality control system, is a suppressor of the Rp21-D21 HR phenotype. ZmCER9, an active E3 ligase, localizes to the ER, consistent with a role in ERAD. It physically interacts with and mediates the proteasome-dependent degradation of both Rp1-D21 and another autoactive Rp1-D derivate but neither interacts with nor affects the protein levels of three non-autoactive Rp1-D derivatives. ZmCER9 also suppresses the activity and directs the degradation of autoactive NLRs from Arabidopsis and barley. We describe a novel, and possibly general, mechanism that specifically degrades activated NLRs to suppress the defense response after activation.

We previously demonstrated that maize (Zea mays) locusvery oil yellow1 (vey1)encodes a putative cis-regulatory expression polymorphism at the magnesium chelatase subunit I gene (akaoil yellow1) that strongly modifies the chlorophyll content of the semi-dominantOy1-N1989mutants. Thevey1allele of Mo17 inbred line reduces chlorophyll content in the mutants leading to reduced photosynthetic output.Oy1-N1989mutants in B73 reached reproductive maturity four days later than wild-type siblings. Enhancement ofOy1-N1989by the Mo17 allele at thevey1QTL delayed maturity further, resulting in detection of a flowering time QTL in two bi-parental mapping populations crossed toOy1-N1989. The near isogenic lines of B73 harboring thevey1allele from Mo17 delayed flowering ofOy1-N1989mutants by twelve days. Just as previously observed for chlorophyll content,vey1had no effect on reproductive maturity in the absence of theOy1-N1989allele. Loss of chlorophyll biosynthesis inOy1-N1989mutants and enhancement byvey1reduced CO2assimilation. We attempted to separate the effects of photosynthesis on the induction of flowering from a possible impact of chlorophyll metabolites and retrograde signaling by manually reducing leaf area. Removal of leaves, independent of theOy1-N1989mutant, delayed flowering but surprisingly reduced chlorophyll contents of emerging leaves. Thus, defoliation did not completely separate the identity of the signal(s) that regulates flowering time from changes in chlorophyll content in the foliage. These findings illustrate the necessity to explore the linkage between metabolism and the mechanisms that connect it to flowering time regulation.