| 1. |
- Bozhkov, Peter, et al.
(författare)
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Transcriptional stimulation of autophagy improves plant fitness
- 2017
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Patent (övrigt vetenskapligt/konstnärligt)abstract
- The present invention provides to a method for enhancing the productivity of a plant by genetically modifying the genome of the plant to over-express at least one autophagy-related (ATG) protein selected from the group consisting of ATG5 and ATG7. The invention further provides a genetically modified plant characterized by over-expression of least one autophagy related (ATG) protein selected from the group consisting of ATG5 and ATG7.Additionally the use of a transgene encoding atleast one autophagy related (ATG) protein selected from the group consisting of ATG5 and ATG7for enhancing the productivity of a plantis disclosed.
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| 2. |
- de Jonge, Jennifer, et al.
(författare)
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Salicylic acid interferes with GFP fluorescence in vivo
- 2017
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Ingår i: Journal of Experimental Botany. - : Oxford University Press (OUP). - 0022-0957 .- 1460-2431. ; 68, s. 1689-1696
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Tidskriftsartikel (refereegranskat)abstract
- Fluorescent proteins have become essential tools for cell biologists. They are routinely used by plant biologists for protein and promoter fusions to infer protein localization, tissue-specific expression and protein abundance. When studying the effects of biotic stress on chromatin, we unexpectedly observed a decrease in GFP signal intensity upon salicylic acid (SA) treatment in Arabidopsis lines expressing histone H1-GFP fusions. This GFP signal decrease was dependent on SA concentration. The effect was not specific to the linker histone H1-GFP fusion but was also observed for the nucleosomal histone H2A-GFP fusion. This result prompted us to investigate a collection of fusion proteins, which included different promoters, subcellular localizations and fluorophores. In all cases, fluorescence signals declined strongly or disappeared after SA application. No changes were detected in GFP-fusion protein abundance when fluorescence signals were lost indicating that SA does not interfere with protein stability but GFP fluorescence. In vitro experiments showed that SA caused GFP fluorescence reduction only in vivo but not in vitro, suggesting that SA requires cellular components to cause fluorescence reduction. Together, we conclude that SA can interfere with the fluorescence of various GFP-derived reporter constructs in vivo. Assays that measure relocation or turnover of GFP-tagged proteins upon SA treatment should therefore be evaluated with caution.
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| 3. |
- Hafrén, Anders, et al.
(författare)
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NBR1-mediated antiviral xenophagy in plant immunity
- 2017
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Ingår i: Autophagy. - : Informa UK Limited. - 1554-8627 .- 1554-8635. ; 13, s. 2000-2001
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Annan publikation (refereegranskat)abstract
- Macroautophagy/autophagy intersects with metazoan virus infections in highly complex and multifaceted ways. Autophagy mechanisms are part of antiviral immunity, but can be manipulated by several viruses to the benefit of infection. In plants, however, the roles of autophagy in virus infections have only recently started to emerge. Here, we present and discuss our recent study that identified 2 prominent functions of autophagy upon cauliflower mosaic virus (CaMV) infection in Arabidopsis. We found that "bulk" autophagy significantly extended the life span of infected plants and increased total virus production. In addition to this proviral role, we discovered that the selective autophagy receptor protein AT4G24690/NBR1 binds viral particles to mediate their xenophagic degradation. Intriguingly, CaMV inclusion bodies protect viral particles from xenophagy and thus represent a sophisticated strategy to counter the antiviral capacity while maintaining the proviral activity of autophagy. Together, our study gives a seminal description of how autophagy is integrated into host immunity and viral pathogenesis in plants, and provides a primary example for removal of a plant pathogen by xenophagy.
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| 4. |
- Hafrén, Anders, et al.
(författare)
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Selective autophagy limits cauliflower mosaic virus infection by NBR1-mediated targeting of viral capsid protein and particles
- 2017
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 114, s. E2026-E2035
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Tidskriftsartikel (refereegranskat)abstract
- Autophagy plays a paramount role in mammalian antiviral immunity including direct targeting of viruses and their individual components, andmany viruses have evolved measures to antagonize or even exploit autophagy mechanisms for the benefit of infection. In plants, however, the functions of autophagy in host immunity and viral pathogenesis are poorly understood. In this study, we have identified both anti-and proviral roles of autophagy in the compatible interaction of cauliflower mosaic virus (CaMV), a double-stranded DNA pararetrovirus, with the model plant Arabidopsis thaliana. We show that the autophagy cargo receptor NEIGHBOR OF BRCA1 (NBR1) targets nonassembled and virus particle-forming capsid proteins to mediate their autophagy-dependent degradation, thereby restricting the establishment of CaMV infection. Intriguingly, the CaMV-induced virus factory inclusions seem to protect against autophagic destruction by sequestering capsid proteins and coordinating particle assembly and storage. In addition, we found that virus-triggered autophagy prevents extensive senescence and tissue death of infected plants in a largely NBR1-independent manner. This survival function significantly extends the timespan of virus production, thereby increasing the chances for virus particle acquisition by aphid vectors and CaMV transmission. Together, our results provide evidence for the integration of selective autophagy into plant immunity against viruses and reveal potential viral strategies to evade and adapt autophagic processes for successful pathogenesis.
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| 5. |
- Hofius, Daniel, et al.
(författare)
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Autophagy as an emerging arena for plant-pathogen interactions
- 2017
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Ingår i: Current Opinion in Plant Biology. - : Elsevier BV. - 1369-5266 .- 1879-0356. ; 38, s. 117-123
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Forskningsöversikt (refereegranskat)abstract
- Autophagy is a highly conserved degradation and recycling process that controls cellular homeostasis, stress adaptation, and programmed cell death in eukaryotes. Emerging evidence indicates that autophagy is a key regulator of plant innate immunity and contributes with both pro-death and pro-survival functions to antimicrobial defences, depending on the pathogenic lifestyle. In turn, several pathogens have co-opted and evolved strategies to manipulate host autophagy pathways to the benefit of infection, while some eukaryotic microbes require their own autophagy machinery for successful pathogenesis. In this review, we present and discuss recent advances that exemplify the important role of pro- and antimicrobial autophagy in plant pathogen interactions.
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| 6. |
- Kock, Teh Ooi, et al.
(författare)
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The RING-Type E3 Ligase XBAT35.2 Is Involved in Cell Death Induction and Pathogen Response
- 2017
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Ingår i: Plant Physiology. - : Oxford University Press (OUP). - 0032-0889 .- 1532-2548. ; 175, s. 1469-1483
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Tidskriftsartikel (refereegranskat)abstract
- XBAT35 belongs to a subfamily of Arabidopsis (Arabidopsis thaliana) RING-type E3s that are similar in domain architecture to the rice (Oryza sativa) XA21 Binding Protein3, a defense protein. The XBAT35 transcript undergoes alternative splicing to produce two protein isoforms, XBAT35.1 and XBAT35.2. Here, we demonstrate that XBAT35.2 localizes predominantly to the Golgi and is involved in cell death induction and pathogen response. XBAT35.2, but not XBAT35.1, was found to trigger cell death when overexpressed in tobacco (Nicotiana benthamiana) leaves and does so in a manner that requires its RING domain. Loss of XBAT35 gene function disrupts the plant's ability to defend against pathogen attack, whereas overexpression of XBAT35.2 enhances resistance to pathogens. XBAT35.2 was found to be unstable and promotes its own degradation, suggesting self-regulation. Inoculation with virulent and avirulent strains of the bacterial pathogen Pseudomonas syringae pv tomato DC3000 results in a drastic reduction in the levels of ubiquitinated XBAT35.2 and an increase in the abundance of the E3. This implies that pathogen infection prohibits XBAT35.2 self-regulation and stabilizes the E3. In agreement with a role in defending against pathogens, XBAT35.2 interacts with defense-related Accelerated Cell Death11 (ACD11) in planta and promotes the proteasome-dependent turnover of ACD11 in cell-free degradation assays. In accordance with regulation by a stabilized XBAT35.2, the levels of ubiquitinated ACD11 increased considerably, and the abundance of ACD11 was reduced following pathogen infection. In addition, treatment of transgenic seedlings with a proteasome inhibitor results in the accumulation of ACD11, confirming proteasome-dependent degradation. Collectively, these results highlight a novel role for XBAT35.2 in cell death induction and defense against pathogens.
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| 7. |
- Üstün, Suayib, et al.
(författare)
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Autophagy as a mediator of life and death in plants
- 2017
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Ingår i: Current Opinion in Plant Biology. - : Elsevier BV. - 1369-5266 .- 1879-0356. ; 40, s. 122-130
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Forskningsöversikt (refereegranskat)abstract
- Autophagy is a major pathway for degradation and recycling of cytoplasmic material, including individual proteins, aggregates, and entire organelles. Autophagic processes serve mainly survival functions in cellular homeostasis, stress adaptation and immune responses but can also have death-promoting activities in different eukaryotic organisms. In plants, the role of autophagy in the regulation of programmed cell death (PCD) remained elusive and a subject of debate. More recent evidence, however, has resulted in the consensus that autophagy can either promote or restrict different forms of PCD. Here, we present latest advances in understanding the molecular mechanisms and functions of plant autophagy and discuss their implications for life and death decisions in the context of developmental and pathogen-induced PCD.
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