An endogenous F-box protein regulates ARGONAUTE1 in Arabidopsis thaliana

Earley, Keith; Smith, Stacy; Weber, Ross A.; Gregory, B. Gloor; Poethig, R. Scott

doi:10.1186/1758-907x-1-15

Cited by 78 publications

(83 citation statements)

References 40 publications

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“…1E). It is noteworthy that in the absence of P0, AGO1 also precipitates CUL1, although less efficiently, suggesting that endogenous SCF-type ubiquitin E3 ligases may also regulate AGO1 as recently proposed (17). Furthermore, we observed an enrichment of polyubiquitin conjugates in AGO1 immunoprecipitates in the presence of P0.…”

Section: Resultssupporting

confidence: 64%

Degradation of the antiviral component ARGONAUTE1 by the autophagy pathway

Derrien

Baumberger

Schepetilnikov

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

255

288

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Posttranscriptional gene silencing (PTGS) mediated by siRNAs is an evolutionarily conserved antiviral defense mechanism in higher plants and invertebrates. In this mechanism, viral-derived siRNAs are incorporated into the RNA-induced silencing complex (RISC) to guide degradation of the corresponding viral RNAs. In Arabidopsis, a key component of RISC is ARGONAUTE1 (AGO1), which not only binds to siRNAs but also carries the RNA slicer activity. At present little is known about posttranslational mechanisms regulating AGO1 turnover. Here we report that the viral suppressor of RNA silencing protein P0 triggers AGO1 degradation by the autophagy pathway. Using a P0-inducible transgenic line, we observed that AGO1 degradation is blocked by inhibition of autophagy. The engineering of a functional AGO1 fluorescent reporter protein further indicated that AGO1 colocalizes with autophagy-related (ATG) protein 8a (ATG8a) positive bodies when degradation is impaired. Moreover, this pathway also degrades AGO1 in a nonviral context, especially when the production of miRNAs is impaired. Our results demonstrate that a selective process such as ubiquitylation can lead to the degradation of a key regulatory protein such as AGO1 by a degradation process generally believed to be unspecific. We anticipate that this mechanism will not only lead to degradation of AGO1 but also of its associated proteins and eventually small RNAs.

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Section: Resultssupporting

confidence: 64%

Degradation of the antiviral component ARGONAUTE1 by the autophagy pathway

Derrien

Baumberger

Schepetilnikov

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

255

288

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“…After growing on Murashige and Skoog (MS) medium containing 30 mM ABA for 5 d, the root length of ago1-27 and the two 35S:MIR168a lines decreased 85%, 70%, and 75%, respectively, compared with a 40% decrease in wild-type plants. These results indicate that disturbance of AGO1 function leads to enhanced sensitivity to exogenous ABA treatment and are consistent with the results of Earley et al (2010).…”

Section: Resultssupporting

confidence: 81%

“…Although several AGO proteins have been shown to regulate biotic stresses (Katiyar-Agarwal et al, 2007;Li et al, 2010;Zhang et al, 2011), the role of AGO proteins in regulating abiotic stress responses is still not well understood. A recent report showed that a decrease in AGO1 confers hypersensitivity to ABA, whereas an increase in the level of AGO1 leads to ABA hyposensitivity (Earley et al, 2010). However, the role of AGO1 in abiotic stress response pathways is still unclear.…”

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confidence: 99%

Transcriptional Regulation of ArabidopsisMIR168aandARGONAUTE1Homeostasis in Abscisic Acid and Abiotic Stress Responses

et al. 2012

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The accumulation of a number of small RNAs in plants is affected by abscisic acid (ABA) and abiotic stresses, but the underlying mechanisms are poorly understood. The miR168-mediated feedback regulatory loop regulates ARGONAUTE1 (AGO1) homeostasis, which is crucial for gene expression modulation and plant development. Here, we reveal a transcriptional regulatory mechanism by which MIR168 controls AGO1 homeostasis during ABA treatment and abiotic stress responses in Arabidopsis (Arabidopsis thaliana). Plants overexpressing MIR168a and the AGO1 loss-of-function mutant ago1-27 display ABA hypersensitivity and drought tolerance, while the mir168a-2 mutant shows ABA hyposensitivity and drought hypersensitivity. Both the precursor and mature miR168 were induced under ABA and several abiotic stress treatments, but no obvious decrease for the target of miR168, AGO1, was shown under the same conditions. However, promoter activity analysis indicated that AGO1 transcription activity was increased under ABA and drought treatments, suggesting that transcriptional elevation of MIR168a is required for maintaining a stable AGO1 transcript level during the stress response. Furthermore, we showed both in vitro and in vivo that the transcription of MIR168a is directly regulated by four abscisic acid-responsive element (ABRE) binding factors, which bind to the ABRE cis-element within the MIR168a promoter. This ABRE motif is also found in the promoter of MIR168a homologs in diverse plant species. Our findings suggest that transcriptional regulation of miR168 and posttranscriptional control of AGO1 homeostasis may play an important and conserved role in stress response and signal transduction in plants.

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“…Moreover, recent work showed that mutations in the F-box protein FBW2 suppress sqn mutations as well as hypomorphic ago1 mutations. In addition, overexpression of FBW2 reduces AGO1 protein levels but not AGO1 mRNA levels, suggesting that FBW2 acts as a negative regulator of AGO1 (Earley et al, 2010).…”

Section: Posttranslational Regulation Of Ago Proteinsmentioning

confidence: 99%