Plant TRAF Proteins Regulate NLR Immune Receptor Turnover

Abstract

In animals, Tumor necrosis factor receptor-associated factor (TRAF) proteins are molecular adaptors that regulate innate and adaptive immunity, development, and abiotic stress responses. Although gene families encoding TRAF domain-containing proteins exhibit enriched diversity in higher plants, their biological roles are poorly defined. Here, we report the identification of two redundant TRAF proteins, Mutant, snc1-enhancing 13 (MUSE13) and MUSE14, that contribute to the turnover of nucleotide-binding domain and leucine-rich repeat-containing (NLR) immune receptors SNC1 and RPS2. Loss of both MUSE13 and MUSE14 leads to enhanced pathogen resistance, NLR accumulation, and autoimmunity, while MUSE13 overexpression results in reduced NLR levels and activity. In planta, MUSE13 associates with SNC1, RPS2, and the E3 ubiquitin ligase SCF(CPR1). Taken together, we speculate that MUSE13 and MUSE14 associate with the SCF E3 ligase complex to form a plant-type TRAFasome, which modulates ubiquitination and subsequent degradation of NLR immune sensors to maintain their homeostasis.

TRAF Family Proteins Regulate Autophagy Dynamics by Modulating AUTOPHAGY PROTEIN6 Stability in Arabidopsis

“…These findings confirm that although the working mechanisms vary, the regulation of TRAF-mediated autophagy is evolutionarily conserved between mammals and plants. Consistent with this notion, a recent report revealed that similar to mammalian TRAFs, Arabidopsis TRAF1a and TRAF1b (termed MUSE14 and MUSE13, respectively, in that study) are involved in regulating plant immunity and pathogen resistance by modulating the homeostasis of NLR immune sensors SNC1 and RPS2 (Huang et al, 2016).…”

“…Phenotypic analyses showed that the dwarfed growth and increased sensitivity to carbon starvation in traf1a/ b-2 were completely rescued by the TRAF1a-FLAG transgene (Supplemental Figures 4A and 4B). Moreover, a recent report demonstrated that the growth defects and autoimmunity phenotype in muse13-2 muse14-1 mutants (traf1a/b in this study) were suppressed by the snc1-r1 mutant (Huang et al, 2016). To uncouple the autophagy deficiency-related phenotypes from the autoimmunity phenotypes in these mutants, we analyzed the response of the snc1-r1 muse13-2 muse14-1 triple mutant (Huang et al, 2016) to nutrient starvation.…”

“…Moreover, a recent report demonstrated that the growth defects and autoimmunity phenotype in muse13-2 muse14-1 mutants (traf1a/b in this study) were suppressed by the snc1-r1 mutant (Huang et al, 2016). To uncouple the autophagy deficiency-related phenotypes from the autoimmunity phenotypes in these mutants, we analyzed the response of the snc1-r1 muse13-2 muse14-1 triple mutant (Huang et al, 2016) to nutrient starvation. When 3-week-old plants were (A) Subcellular localization of GFP-TRAF1a and TRAF1b-GFP in Arabidopsis protoplasts under constant light (LL) or dark (DD) conditions.…”

“…The Arabidopsis genome contains more than 70 genes encoding TRAF domain-containing proteins (Oelmüller et al, 2005;Huang et al, 2016), but few of their functions have been characterized to date. To isolate TRAF family proteins with potential roles in autophagy, we cloned half of the TRAF family genes and fused them to GFP for transient expression in Arabidopsis protoplasts.…”

“…Since these two proteins contain a single TRAF domain and their structures resemble that of mammalian TRAF1, we designated these proteins TRAF1a (At5g43560) and TRAF1b (At1g04300). These proteins were originally named MUSE14 and MUSE13, respectively (MUTANT, SNC1-ENHANCING 14; Huang et al, 2016), but we suggest renaming them to reflect their membership in the TRAF family.…”