The KEEP ON GOING Protein of <i>Arabidopsis</i> Regulates Intracellular Protein Trafficking and Is Degraded during Fungal Infection

Gu, Yangnan; Innes, Roger W.

doi:10.1105/tpc.112.105254

Cited by 83 publications

(76 citation statements)

References 74 publications

(139 reference statements)

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“…2G). This corresponds to the reported extranuclear localization of KEG-GFP (Gu and Innes, 2011) and the localization of the interaction between KEG and ENHANCED DISEASE RESISTANCE1 (EDR1; Gu and Innes, 2012) and between KEG and ABI5 . Coexpression of NINJA-nGFP led to a nuclear signal (Fig.…”

Section: Keg Interacts Specifically With Jaz12supporting

confidence: 87%

“…ABA treatment, however, promotes KEG self-ubiquitination and degradation, leading to an increase in ABI5 levels (Liu and Stone, 2010). Intriguingly, in contrast to the nuclear ABI5 subcellular localization, KEG is present in the trans-Golgi network (TGN; Gu and Innes, 2011) and is proposed to be a regulator of post-Golgi trafficking, including the secretion of apoplastic defense proteins (Gu and Innes, 2012). However, when inactivating the RING domain of KEG or mutating a conserved Lys in ABI5, an interaction between KEG and ABI5 can be observed outside the nucleus in the cytoplasm and at the TGN .…”

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confidence: 99%

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The RING E3 Ligase KEEP ON GOING Modulates JASMONATE ZIM-DOMAIN12 Stability

et al. 2015

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Jasmonate (JA) signaling in plants is mediated by the JASMONATE ZIM-DOMAIN (JAZ) proteins that repress the activity of several transcription factors regulating JA-inducible gene expression. The hormone JA-isoleucine triggers the interaction of JAZ repressor proteins with the F-box protein CORONATINE INSENSITIVE1 (COI1), part of an S-phase kinase-associated protein1/Cullin1/F-box protein COI1 (SCF COI1 ) E3 ubiquitin ligase complex, and their degradation by the 26S proteasome. In Arabidopsis (Arabidopsis thaliana), the JAZ family consists of 13 members. The level of redundancy or specificity among these members is currently not well understood. Here, we characterized JAZ12, encoded by a highly expressed JAZ gene. JAZ12 interacted with the transcription factors MYC2, MYC3, and MYC4 in vivo and repressed MYC2 activity. Using tandem affinity purification, we found JAZ12 to interact with SCF COI1 components, matching with observed in vivo ubiquitination and with rapid degradation after treatment with JA. In contrast to the other JAZ proteins, JAZ12 also interacted directly with the E3 RING ligase KEEP ON GOING (KEG), a known repressor of the ABSCISIC ACID INSENSITIVE5 transcription factor in abscisic acid signaling. To study the functional role of this interaction, we circumvented the lethality of keg loss-of-function mutants by silencing KEG using an artificial microRNA approach. Abscisic acid treatment promoted JAZ12 degradation, and KEG knockdown led to a decrease in JAZ12 protein levels. Correspondingly, KEG overexpression was capable of partially inhibiting COI1-mediated JAZ12 degradation. Our results provide additional evidence for KEG as an important factor in plant hormone signaling and a positive regulator of JAZ12 stability.

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Section: Keg Interacts Specifically With Jaz12supporting

confidence: 87%

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confidence: 99%

The RING E3 Ligase KEEP ON GOING Modulates JASMONATE ZIM-DOMAIN12 Stability

et al. 2015

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“…The localization patterns of ATL1 in both transient and stable expression systems mirror those of a typical plasma membrane protein that undergoes constitutive endocytic trafficking, such as BRI1 (Geldner et al, 2007;Geldner and Robatzek, 2008;Kleine-Vehn et al, 2008;Gu and Innes, 2012). Therefore, we conclude that ATL1 is a membrane-associated E3 ligase that constitutively cycles between the plasma membrane and TGN/EE and after internalization can follow a retrograde transport pathway to the MVB/LE and eventually to the lytic vacuole for turnover.…”

Section: Atl1 Undergoes Constitutive Internalization and Vacuolar Degsupporting

confidence: 51%

TheArabidopsisEDR1 Protein Kinase Negatively Regulates the ATL1 E3 Ubiquitin Ligase to Suppress Cell Death

Serrano

Dong

et al. 2014

Plant Cell

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Loss-of-function mutations in the Arabidopsis thaliana ENHANCED DISEASE RESISTANCE1 (EDR1) gene confer enhanced programmed cell death under a variety of abiotic and biotic stress conditions. All edr1 mutant phenotypes can be suppressed by missense mutations in the KEEP ON GOING gene, which encodes a trans-Golgi network/early endosome (TGN/EE)-localized E3 ubiquitin ligase. Here, we report that EDR1 interacts with a second E3 ubiquitin ligase, ARABIDOPSIS TOXICOS EN LEVADURA1 (ATL1), and negatively regulates its activity. Overexpression of ATL1 in transgenic Arabidopsis induced severe growth inhibition and patches of cell death, while transient overexpression in Nicotiana benthamiana leaves induced cell death and tissue collapse. The E3 ligase activity of ATL1 was required for both of these processes. Importantly, we found that ATL1 interacts with EDR1 on TGN/EE vesicles and that EDR1 suppresses ATL1-mediated cell death in N. benthamiana and Arabidopsis. Lastly, knockdown of ATL1 expression suppressed cell death phenotypes associated with the edr1 mutant and made Arabidopsis hypersusceptible to powdery mildew infection. Taken together, our data indicate that ATL1 is a positive regulator of programmed cell death and EDR1 negatively regulates ATL1 activity at the TGN/EE and thus controls stress responses initiated by ATL1-mediated ubiquitination events.

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“…KEG plays a critical role in multiple intracellular trafficking processes, including vacuole biogenesis, targeting of membrane-associated proteins to the vacuole, and secretion of apoplastic proteins (Gu and Innes, 2012). Mutation of KEG specifically suppresses edr1-mediated resistance, but how KEG affects edr1-mediated defenses remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…KEG interacts with EDR1 and recruits it to the trans-Golgi network/early endosome (TGN/EE) vesicles (Wawrzynska et al, 2008;Gu and Innes, 2011). KEG regulates endomembrane protein trafficking and is degraded specifically in cells infected by powdery mildew (Gu and Innes, 2012). Recent work showed that EDR1 also interacts with ARABIDOPSIS TOXICOS EN LEVADURA1 (ATL1), an E3 ubiquitin ligase that positively regulates resistance and cell death.…”

Section: Introductionmentioning

confidence: 99%

ENHANCED DISEASE RESISTANCE4 Associates with CLATHRIN HEAVY CHAIN2 and Modulates Plant Immunity by Regulating Relocation of EDR1 in Arabidopsis

Liu

Zhao

et al. 2015

The Plant Cell

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Obligate biotrophs, such as the powdery mildew pathogens, deliver effectors to the host cell and obtain nutrients from the infection site. The interface between the plant host and the biotrophic pathogen thus represents a major battleground for plant-pathogen interactions. Increasing evidence shows that cellular trafficking plays an important role in plant immunity. Here, we report that Arabidopsis thaliana ENHANCED DISEASE RESISTANCE4 (EDR4) plays a negative role in resistance to powdery mildew and that the enhanced disease resistance in edr4 mutants requires salicylic acid signaling. EDR4 mainly localizes to the plasma membrane and endosomal compartments. Genetic analyses show that EDR4 and EDR1 function in the same genetic pathway. EDR1 and EDR4 accumulate at the penetration site of powdery mildew infection, and EDR4 physically interacts with EDR1, recruiting EDR1 to the fungal penetration site. In addition, EDR4 interacts with CLATHRIN HEAVY CHAIN2 (CHC2), and edr4 mutants show reduced endocytosis rates. Taken together, our data indicate that EDR4 associates with CHC2 and modulates plant immunity by regulating the relocation of EDR1 in Arabidopsis.

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The KEEP ON GOING Protein of Arabidopsis Regulates Intracellular Protein Trafficking and Is Degraded during Fungal Infection

Cited by 83 publications

References 74 publications

The RING E3 Ligase KEEP ON GOING Modulates JASMONATE ZIM-DOMAIN12 Stability

The RING E3 Ligase KEEP ON GOING Modulates JASMONATE ZIM-DOMAIN12 Stability

TheArabidopsisEDR1 Protein Kinase Negatively Regulates the ATL1 E3 Ubiquitin Ligase to Suppress Cell Death

ENHANCED DISEASE RESISTANCE4 Associates with CLATHRIN HEAVY CHAIN2 and Modulates Plant Immunity by Regulating Relocation of EDR1 in Arabidopsis

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