Plant-microbe interaction
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Consequences of flagellin export through the type III secretion system of Pseudomonas syringae reveal a major difference in the innate immune systems of mammals and the model plant Nicotiana bentha...

Consequences of flagellin export through the type III secretion system of Pseudomonas syringae reveal a major difference in the innate immune systems of mammals and the model plant Nicotiana bentha... | Plant-microbe interaction | Scoop.it
Summary
Bacterial flagellin is perceived as a microbe (or pathogen)-associated molecular pattern (MAMP or PAMP) by the extracellular pattern recognition receptors, FLS2 and TLR5, of plants and mammals, respectively.

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Plant-microbe interaction
Current research on plant immunity, effector proteins, the proteasome and autophagy
Curated by Suayib Üstün
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Autophagy as a mediator of life and death in plants

Autophagy as a mediator of life and death in plants | Plant-microbe interaction | Scoop.it
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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Turnip mosaic virus counteracts selective autophagy of the viral silencing suppressor HCpro

Turnip mosaic virus counteracts selective autophagy of the viral silencing suppressor HCpro | Plant-microbe interaction | Scoop.it
Autophagy is a conserved intracellular degradation pathway and has emerged as a key mechanism of antiviral immunity in metazoans, including the selective elimination of viral components. In turn, some animal viruses are able to escape and modulate autophagy for enhanced pathogenicity. Whether host autophagic responses and viral countermeasures play similar roles in plant-virus interactions is not well understood. Here, we have identified selective autophagy as antiviral pathway during plant infection with turnip mosaic virus (TuMV), a positive-stranded RNA potyvirus. We show that the autophagy cargo receptor NBR1 suppresses viral accumulation by targeting the viral RNA silencing suppressor HCpro, presumably in association with virus-induced RNA granules. Intriguingly, TuMV seems to antagonize NBR1-dependent autophagy during infection by the activity of distinct viral proteins, thereby limiting its antiviral capacity. We also found that NBR1-independent bulk autophagy prevents premature plant death, thus extending the life span of virus reservoirs and particle production. Together, our study highlights a conserved role of selective autophagy in antiviral immunity, and suggests the evolvement of viral protein functions to inhibit autophagy processes, despite a potential trade-off in host survival.
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Rescooped by Suayib Üstün from Microbiome and plant immunity
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Root transcriptional dynamics induced by beneficial rhizobacteria and microbial immune elicitors reveal signatures of adaptation to mutualists

Root transcriptional dynamics induced by beneficial rhizobacteria and microbial immune elicitors reveal signatures of adaptation to mutualists | Plant-microbe interaction | Scoop.it
Belowground, microbe-associated molecular patterns (MAMPs) of root-associated microbiota can trigger costly defenses at the expense of plant growth. However, beneficial rhizobacteria, such as Pseudomonas simiae WCS417, promote plant growth and induce systemic resistance without being warded off by local root immune responses. To investigate early root responses that facilitate WCS417 to exert its plant-beneficial functions, we performed time-series RNA-Seq of Arabidopsis roots in response to live WCS417 and compared it to MAMPs flg22417 (from WCS417), flg22Pa (from pathogenic Pseudomonas aeruginosa), and fungal chitin. The MAMP transcriptional responses differed in timing, but displayed a large overlap in gene identity. MAMP-upregulated genes are enriched for genes with functions in immunity, while downregulated genes are enriched for genes related to growth and development. Although 74% of the transcriptional changes inflicted by live WCS417 overlapped with the flg22417 profile, WCS417 actively suppressed more than half of the MAMP-triggered transcriptional responses, possibly to allow the establishment of a mutually beneficial interaction with the host root. Interestingly, the sector of the flg22417-triggered transcriptional network that is suppressed by WCS417 has a strong auxin signature. Using auxin response mutant tir1afb2afb3, we demonstrate a dual role for auxin signaling in finely balancing growth-promoting and defense eliciting activities of beneficial microbes in plant roots.

Via Giannis Stringlis
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The replication initiator protein of a geminivirus interacts with host monoubiquitination machinery and stimulates transcription of the viral genome

The replication initiator protein of a geminivirus interacts with host monoubiquitination machinery and stimulates transcription of the viral genome | Plant-microbe interaction | Scoop.it
Geminiviruses constitute a group of plant viruses, with a ssDNA genome, whose replication in the nucleus of an infected cell requires the function of geminivirus-encoded replication initiator protein (Rep). Our results suggest that monoubiquitinated histone 2B (H2B-ub) promotes tri-methylation of histone 3 at lysine 4 (H3-K4me3) on the promoter of chilli leaf curl virus. We isolated homologues of two major components of the monoubiquitination machinery: UBIQUITIN-CONJUGATING ENZYME2 (NbUBC2) and HISTONE MONOUBIQUITINATION1 (NbHUB1) from N. benthamiana. ChiLCV failed to cause disease in NbUBC2-, and NbHUB1-silenced plants, at the same time, H2B-ub and H3-K4me3 modifications were decreased, and the occupancy of RNA polymerase II on the viral promoter was reduced as well. In further investigations, Rep protein of ChiLCV was found to re-localize NbUBC2 from the cytoplasm to the nucleoplasm, like NbHUB1, the cognate partner of NbUBC2. Rep was observed to interact and co-localize with NbHUB1 and NbUBC2 in the nuclei of the infected cells. In summary, the current study reveals that the ChiLCV Rep protein binds the viral genome and interacts with NbUBC2 and NbHUB1 for the monoubiquitination of histone 2B that subsequently promotes trimethylation of histone 3 at lysine 4 on ChiLCV mini-chromosomes and enhances transcription of the viral genes.
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PNAS: NLR network mediates immunity to diverse plant pathogens (2017)

PNAS: NLR network mediates immunity to diverse plant pathogens (2017) | Plant-microbe interaction | Scoop.it

Both plants and animals rely on nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins to respond to invading pathogens and activate immune responses. An emerging concept of NLR function is that “sensor” NLR proteins are paired with “helper” NLRs to mediate immune signaling. However, our fundamental knowledge of sensor/helper NLRs in plants remains limited. In this study, we discovered a complex NLR immune network in which helper NLRs in the NRC (NLR required for cell death) family are functionally redundant but display distinct specificities toward different sensor NLRs that confer immunity to oomycetes, bacteria, viruses, nematodes, and insects. The helper NLR NRC4 is required for the function of several sensor NLRs, including Rpi-blb2, Mi-1.2, and R1, whereas NRC2 and NRC3 are required for the function of the sensor NLR Prf. Interestingly, NRC2, NRC3, and NRC4 redundantly contribute to the immunity mediated by other sensor NLRs, including Rx, Bs2, R8, and Sw5. NRC family and NRC-dependent NLRs are phylogenetically related and cluster into a well-supported superclade. Using extensive phylogenetic analysis, we discovered that the NRC superclade probably emerged over 100 Mya from an NLR pair that diversified to constitute up to one-half of the NLRs of asterids. These findings reveal a complex genetic network of NLRs and point to a link between evolutionary history and the mechanism of immune signaling. We propose that this NLR network increases the robustness of immune signaling to counteract rapidly evolving plant pathogens.


Via Kamoun Lab @ TSL
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Rescooped by Suayib Üstün from Plant immunity and legume symbiosis
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A bacterial acetyltransferase triggers immunity in Arabidopsis thaliana independent of hypersensitive response

A bacterial acetyltransferase triggers immunity in Arabidopsis thaliana independent of hypersensitive response | Plant-microbe interaction | Scoop.it

Type-III secreted effectors (T3Es) play critical roles during bacterial pathogenesis in plants. Plant recognition of certain T3Es can trigger defence, often accompanied by macroscopic cell death, termed the hypersensitive response (HR). Economically important species of kiwifruit are susceptible to Pseudomonas syringae pv. actinidiae (Psa), the causal agent of kiwifruit bacterial canker. Although Psa is non-pathogenic in Arabidopsis thaliana, we observed that a T3E, HopZ5 that is unique to a global outbreak clade of Psa, triggers HR and defence in Arabidopsis accession Ct-1. Ws-2 and Col-0 accessions are unable to produce an HR in response to Pseudomonas-delivered HopZ5. While Ws-2 is susceptible to virulent bacterial strain Pseudomonas syringae pv. tomato DC3000 carrying HopZ5, Col-0 is resistant despite the lack of an HR. We show that HopZ5, like other members of the YopJ superfamily of acetyltransferases that it belongs to, autoacetylates lysine residues. Through comparisons to other family members, we identified an acetyltransferase catalytic activity and demonstrate its requirement for triggering defence in Arabidopsis and Nicotiana species. Collectively, data herein indicate that HopZ5 is a plasma membrane-localized acetyltransferase with autoacetylation activity required for avirulence.


Via Christophe Jacquet
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Rescooped by Suayib Üstün from Plant immunity and legume symbiosis
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Autophagy as an emerging arena for plant–pathogen interactions

Autophagy as an emerging arena for plant–pathogen interactions | Plant-microbe interaction | Scoop.it

Highlights

• Autophagy is an integral part of plant–pathogen interactions.
• A large variety of microbial pathogens target or are targeted by plant autophagy.
• Autophagy in eukaryotic microbial pathogens is essential for pathogenesis.
• Plant autophagy participates in defense responses against invading microbes.
• Successful pathogens have evolved strategies to manipulate plant autophagy.



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.


Via Christophe Jacquet
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An Oomycete Effector Protein Induces Shade Avoidance In Arabidopsis And Attenuates Salicylate Signaling By Binding To Host Proteins Of The RADICAL-INDUCED CELL DEATH1 Family

An Oomycete Effector Protein Induces Shade Avoidance In Arabidopsis And Attenuates Salicylate Signaling By Binding To Host Proteins Of The RADICAL-INDUCED CELL DEATH1 Family | Plant-microbe interaction | Scoop.it
The oomycete pathogen Hyaloperonospora arabidopsidis (Hpa) causes downy mildew disease on Arabidopsis. During infection, Hpa like other biotrophic pathogens, suppresses activation of plant innate immunity by translocating effector proteins into host cells. Some of these effectors localize to the host cell nucleus where they may manipulate transcriptional reprogramming of plant defense genes. Here we report that the nuclear-localized Hpa effector HaRxL106, when expressed in Arabidopsis, induces shade avoidance and attenuates the transcriptional response to the defense signaling molecule salicylic acid. HaRxL106 interacts with RADICAL-INDUCED CELL DEATH1 (RCD1) and loss of RCD1 function renders Arabidopsis resilient against HaRxL106-mediated suppression of immunity. To further characterize the molecular functions of RCD1 we solved a crystal structure of the RCD1 Poly-(ADP-ribose)-Polymerase (PARP) domain and, based on non-conservation of amino acids constituting the active site of canonical PARPs, conclude that RCD1 has no PARP activity. We report that RCD1-type proteins are phosphorylated and identified histone-modifying Mut9-like kinases (MLKs) as RCD1-interacting proteins. A mlk1,3,4 triple mutant exhibits stronger SA-induced defense marker gene expression compared to wild-type plants. Our data suggest that HaRxL106 suppresses Arabidopsis innate immunity by manipulating the function(s) of RCD1 in the host cell nucleus and point towards a role of RCD1 as a transcriptional co-regulator that integrates signals from light and pathogen sensors.
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Translatome analysis of an NB-LRR immune response identifies important contributors to plant immunity in Arabidopsis | Journal of Experimental Botany | Oxford Academic

Translatome analysis of an NB-LRR immune response identifies important contributors to plant immunity in Arabidopsis | Journal of Experimental Botany | Oxford Academic | Plant-microbe interaction | Scoop.it
An important branch of plant immunity involves the recognition of pathogens by nucleotide-binding, leucine-rich repeat (NB-LRR) proteins. However, signaling events downstream of NB-LRR activation are poorly understood. We have analysed the Arabidopsis translatome using ribosome affinity purification and RNA sequencing. Our results show that the translational status of hundreds of transcripts is differentially affected upon activation of the NB-LRR protein RPM1, showing an overall pattern of a switch away from growth-related activities to defense. Among these is the central translational regulator and growth promoter, Target of Rapamycin (TOR) kinase. Suppression of TOR expression leads to increased resistance to pathogens while overexpression of TOR results in increased susceptibility, indicating an important role for translational control in the switch from growth to defense. Furthermore, we show that several additional genes whose mRNAs are translationally regulated, including BIG, CCT2, and CIPK5, are required for both NB-LRR-mediated and basal plant innate immunity, identifying novel actors in plant defense.

Via Christophe Jacquet
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Elucidation of the anti-autophagy mechanism of the Legionella effector RavZ using semisynthetic LC3 proteins

Elucidation of the anti-autophagy mechanism of the Legionella effector RavZ using semisynthetic LC3 proteins | Plant-microbe interaction | Scoop.it
Autophagy is a conserved cellular process involved in the elimination of proteins and organelles. It is also used to combat infection with pathogenic microbes. The intracellular pathogen Legionella pneumophila manipulates autophagy by delivering the effector protein RavZ to deconjugate Atg8/LC3 proteins coupled to phosphatidylethanolamine (PE) on autophagosomal membranes. To understand how RavZ recognizes and deconjugates LC3-PE, we prepared semisynthetic LC3 proteins and elucidated the structures of the RavZ:LC3 interaction. Semisynthetic LC3 proteins allowed the analysis of structure-function relationships. RavZ extracts LC3-PE from the membrane before deconjugation. RavZ initially recognizes the LC3 molecule on membranes via its N-terminal LC3-interacting region (LIR) motif. The RavZ α3 helix is involved in extraction of the PE moiety and docking of the acyl chains into the lipid-binding site of RavZ that is related in structure to that of the phospholipid transfer protein Sec14. Thus, Legionella has evolved a novel mechanism to specifically evade host autophagy.
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Selective Autophagy of BES1 Mediated by DSK2 Balances Plant Growth and Survival

Selective Autophagy of BES1 Mediated by DSK2 Balances Plant Growth and Survival | Plant-microbe interaction | Scoop.it
Plants encounter a variety of stresses and must fine-tune their growth and stress-response programs to best suit their environment. BES1 functions as a master regulator in the brassinosteroid (BR) pathway that promotes plant growth. Here, we show that BES1 interacts with the ubiquitin receptor protein DSK2 and is targeted to the autophagy pathway during stress via the interaction of DSK2 with ATG8, a ubiquitin-like protein directing autophagosome formation and cargo recruitment. Additionally, DSK2 is phosphorylated by the GSK3-like kinase BIN2, a negative regulator in the BR pathway. BIN2 phosphorylation of DSK2 flanking its ATG8 interacting motifs (AIMs) promotes DSK2-ATG8 interaction, thereby targeting BES1 for degradation. Accordingly, loss-of-function dsk2 mutants accumulate BES1, have altered global gene expression profiles, and have compromised stress responses. Our results thus reveal that plants coordinate growth and stress responses by integrating BR and autophagy pathways and identify the molecular basis of this crosstalk.
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Keap1/Cullin3 Modulates p62/SQSTM1 Activity via UBA Domain Ubiquitination

Keap1/Cullin3 Modulates p62/SQSTM1 Activity via UBA Domain Ubiquitination | Plant-microbe interaction | Scoop.it
p62/SQSTM1 (p62) is a scaffolding protein that facilitates the formation and degradation of ubiquitinated aggregates via its self-interaction and ubiquitin binding domains. The regulation of this process is unclear but may relate to the post-translational modification of p62. In the present study, we find that Keap1/Cullin3 ubiquitinates p62 at lysine 420 within its UBA domain. Substitution of lysine 420 with an arginine diminishes p62 sequestration and degradation activity similar what is seen when the UBA domain is deleted. Overexpression of Keap1/Cullin3 in p62-WT-expressing cells increases ubiquitinated inclusion formation and p62's association with LC3 and rescues proteotoxicity. This effect is not seen in cells expressing a mutant p62 that fails to interact with Keap1. Interestingly, p62 disease mutants have diminished or absent UBA domain ubiquitination. These data suggest that the ubiquitination of p62’s UBA domain at lysine 420 may regulate p62’s function and be disrupted in p62-associated disease.
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TRAF-Family Proteins Regulate Autophagy Dynamics by Modulating AUTOPHAGY PROTEIN6 Stability in Arabidopsis

TRAF-Family Proteins Regulate Autophagy Dynamics by Modulating AUTOPHAGY PROTEIN6 Stability in Arabidopsis | Plant-microbe interaction | Scoop.it
Eukaryotic cells use autophagy to recycle cellular components. During autophagy, autophagosomes deliver cytoplasmic contents to the vacuole or lysosome for breakdown. Mammalian cells regulate the dynamics of autophagy via ubiquitin-mediated proteolysis of autophagy proteins. Here, we show that the Arabidopsis thaliana Tumor necrosis factor Receptor-Associated Factor (TRAF)-family proteins, TRAF1a and TRAF1b (previously named MUSE14 and MUSE13, respectively) help regulate autophagy via ubiquitination. Upon starvation, cytoplasmic TRAF1a and TRAF1b translocated to autophagosomes. Knockout traf1a/b lines showed reduced tolerance to nutrient deficiency, increased salicylic acid and reactive oxygen species levels, and constitutive cell death in rosettes, resembling the phenotypes of autophagy-defective mutants. Starvation-activated autophagosome accumulation decreased in traf1a/b root cells, indicating that TRAF1a and TRAF1b function redundantly in regulating autophagosome formation. TRAF1a and TRAF1b interacted in planta with ATG6 and the RING finger E3 ligases SINAT1, SINAT2, and SINAT6 (with a truncated RING-finger domain). SINAT1 and SINAT2 require the presence of TRAF1a and TRAF1b to ubiquitinate and destabilize AUTOPHAGY PROTEIN6 (ATG6) in vivo. Conversely, starvation-induced SINAT6 reduced SINAT1- and SINAT2-mediated ubiquitination and degradation of ATG6. Consistently, SINAT1/SINAT2 and SINAT6 knockout mutants exhibited increased tolerance and sensitivity, respectively, to nutrient starvation. Therefore, TRAF1a and TRAF1b function as molecular adaptors that help regulate autophagy by modulating ATG6 stability in Arabidopsis.
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A Bacterial Type III Effector Targets the Master Regulator of Salicylic Acid Signaling, NPR1, to Subvert Plant Immunity

A Bacterial Type III Effector Targets the Master Regulator of Salicylic Acid Signaling, NPR1, to Subvert Plant Immunity | Plant-microbe interaction | Scoop.it
NPR1, as the key transcriptional regulator of salicylic acid signaling, plays a pivotal
role in plant local and systemic immunity. Chen et al. find that Pseudomonas syringae
type III effector AvrPtoB directly targets the activated form of NPR1 for ubiquitination-mediated
degradation to inhibit target gene expression, thereby dampening plant immunity.

Via Tatsuya Nobori, Jim Alfano
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bioRxiv: The plant calcium-dependent protein kinase CPK3 phosphorylates REM1.3 to restrict viral infection (2017)

bioRxiv: The plant calcium-dependent protein kinase CPK3 phosphorylates REM1.3 to restrict viral infection (2017) | Plant-microbe interaction | Scoop.it

Plants respond to pathogens through dynamic regulation of plasma membrane-bound signaling pathways. To date, how the plant plasma membrane is involved in responses to viruses is mostly unknown. Here, we show that plant cells sense the Potato virus X (PVX) COAT PROTEIN and TRIPLE GENE BLOCK 1 proteins and subsequently trigger the activation of a membrane-bound calcium-dependent kinase. We show that the Arabidopsis thaliana CALCIUM-DEPENDENT PROTEIN KINASE 3-interacts with group 1 REMORINs in vivo, phosphorylates the intrinsically disordered N-terminal domain of the Group 1 REMORIN REM1.3, and restricts PVX cell-to-cell movement. REM1.3's phospho-status defines its plasma membrane nanodomain organization and is crucial for REM1.3-dependent restriction of PVX cell-to-cell movement by regulation of callose deposition at plasmodesmata. This study unveils plasma membrane nanodomain-associated molecular events underlying the plant immune response to viruses.


Via The Sainsbury Lab, Kamoun Lab @ TSL
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The Sainsbury Lab's curator insight, October 23, 5:16 AM
Plants respond to pathogens through dynamic regulation of plasma membrane-bound signaling pathways. To date, how the plant plasma membrane is involved in responses to viruses is mostly unknown. Here, we show that plant cells sense the Potato virus X (PVX) COAT PROTEIN and TRIPLE GENE BLOCK 1 proteins and subsequently trigger the activation of a membrane-bound calcium-dependent kinase. We show that the Arabidopsis thaliana CALCIUM-DEPENDENT PROTEIN KINASE 3-interacts with group 1 REMORINs in vivo, phosphorylates the intrinsically disordered N-terminal domain of the Group 1 REMORIN REM1.3, and restricts PVX cell-to-cell movement. REM1.3's phospho-status defines its plasma membrane nanodomain organization and is crucial for REM1.3-dependent restriction of PVX cell-to-cell movement by regulation of callose deposition at plasmodesmata. This study unveils plasma membrane nanodomain-associated molecular events underlying the plant immune response to viruses.
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Assembly and Function of Heterotypic Ubiquitin Chains in Cell-Cycle and Protein Quality Control

Assembly and Function of Heterotypic Ubiquitin Chains in Cell-Cycle and Protein Quality Control | Plant-microbe interaction | Scoop.it
Posttranslational modification with ubiquitin chains controls cell fate in all eukaryotes. Depending on the connectivity between subunits, different ubiquitin chain types trigger distinct outputs, as seen with K48- and K63-linked conjugates that drive protein degradation or complex assembly, respectively. Recent biochemical analyses also suggested roles for mixed or branched ubiquitin chains, yet without a method to monitor endogenous conjugates, the physiological significance of heterotypic polymers remained poorly understood. Here, we engineered a bispecific antibody to detect K11/K48-linked chains and identified mitotic regulators, misfolded nascent polypeptides, and pathological Huntingtin variants as their endogenous substrates. We show that K11/K48-linked chains are synthesized and processed by essential ubiquitin ligases and effectors that are mutated across neurodegenerative diseases; accordingly, these conjugates promote rapid proteasomal clearance of aggregation-prone proteins. By revealing key roles of K11/K48-linked chains in cell-cycle and quality control, we establish heterotypic ubiquitin conjugates as important carriers of biological information.
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Stop blocking postdocs’ paths to success

Stop blocking postdocs’ paths to success | Plant-microbe interaction | Scoop.it
One type of postdoc maltreatment is rarely discussed, despite its prevalence and importance — should a postdoc be able to take their research project with them when they set up their own lab? And if so, should that new principal investigator (PI) be free from direct competition on that project with his or her former mentor? In my view, the answer to both questions is yes. Such 'project porting' is crucial for the success of young scientists and should be a fundamental right for postdocs.

This is such a touchy topic that it is only now that I feel comfortable writing about it. I am at the end of a long academic career and dying of stage four pancreatic cancer. I think it's time for the academic community to start openly discussing the issue of research freedom for postdocs (or lack of it).

Opinions will vary, but different strategies could enable PIs and postdocs to handle the issue more constructively. At the very least, trainees looking for a postdoc job need to find out about the policies of potential mentors before selecting a lab, and assess the implications that these policies could have for their independent success.

Via Francis Martin
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MAPK-triggered chromatin reprogramming by histone deacetylase in plant innate immunity

MAPK-triggered chromatin reprogramming by histone deacetylase in plant innate immunity | Plant-microbe interaction | Scoop.it
Background

Microbial-associated molecular patterns activate several MAP kinases, which are major regulators of the innate immune response in Arabidopsis thaliana that induce large-scale changes in gene expression. Here, we determine whether microbial-associated molecular pattern-triggered gene expression involves modifications at the chromatin level.
Results

Histone acetylation and deacetylation are major regulators of microbial-associated molecular pattern-triggered gene expression and implicate the histone deacetylase HD2B in the reprogramming of defence gene expression and innate immunity. The MAP kinase MPK3 directly interacts with and phosphorylates HD2B, thereby regulating the intra-nuclear compartmentalization and function of the histone deacetylase.
Conclusions

By studying a number of gene loci that undergo microbial-associated molecular pattern-dependent activation or repression, our data reveal a mechanistic model for how protein kinase signaling directly impacts chromatin reprogramming in plant defense.

Via Christophe Jacquet
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Direct and Indirect Visualization of Bacterial Effector Delivery into Diverse Plant Cell Types During Infection

Direct and Indirect Visualization of Bacterial Effector Delivery into Diverse Plant Cell Types During Infection | Plant-microbe interaction | Scoop.it
To cause disease, diverse pathogens deliver effector proteins into host cells. Pathogen effectors can inhibit defense responses, alter host physiology, and represent important cellular probes to investigate plant biology. However, effector function and localization have primarily been investigated after overexpression in planta. Visualizing effector delivery during infection is challenging due to the plant cell wall, autofluorescence, and low effector abundance. Here, we utilized a GFP strand system to directly visualize bacterial effectors delivered into plant cells through the Type III secretion system. GFP is a beta barrel that can be divided into 11 strands. We generated transgenic Arabidopsis thaliana plants expressing GFP1-10 (strands 1 to 10). Multiple bacterial effectors tagged with the complementary strand 11 epitope retained their biological function in Arabidopsis and tomato (Solanum lycopersicum). Infection of plants expressing GFP1-10 with bacteria delivering GFP11-tagged effectors enabled direct effector detection in planta. We investigated the temporal and spatial delivery of GFP11-tagged effectors during infection with the foliar pathogen Pseudomonas syringae and the vascular pathogen Ralstonia solanacearum. Thus, the GFP strand system can be broadly used to investigate effector biology in planta.
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Receptor oligomerization guides pathway choice between proteasomal and autophagic degradation : Nature Cell Biology : Nature Research

Receptor oligomerization guides pathway choice between proteasomal and autophagic degradation : Nature Cell Biology : Nature Research | Plant-microbe interaction | Scoop.it

Abnormal or aggregated proteins have a strong cytotoxic potential and are causative for human disorders such as Alzheimer’s, Parkinson’s, Huntington’s disease and amyotrophic lateral sclerosis. If not restored by molecular chaperones, abnormal proteins are typically degraded by proteasomes or eliminated by selective autophagy. The discovery that both pathways are initiated by substrate ubiquitylation but utilize different ubiquitin receptors incited a debate over how pathway choice is achieved. Here, we demonstrate in yeast that pathway choice is made after substrate ubiquitylation by competing ubiquitin receptors harbouring either proteasome- or autophagy-related protein 8 (Atg8/LC3)-binding modules. Proteasome pathway receptors bind ubiquitin moieties more efficiently, but autophagy receptors gain the upper hand following substrate aggregation and receptor bundling. Indeed, by using sets of modular artificial receptors harbouring identical ubiquitin-binding modules we found that proteasome/autophagy pathway choice is independent of the ubiquitin-binding properties of the receptors but largely determined by their oligomerization potentials. Our work thus suggests that proteasomal degradation and selective autophagy are two branches of an adaptive protein quality control pathway, which uses substrate ubiquitylation as a shared degradation signal.

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Frontiers | A Proteomic Approach Suggests Unbalanced Proteasome Functioning Induced by the Growth-Promoting Bacterium Kosakonia radicincitans in Arabidopsis | Plant Science

Frontiers | A Proteomic Approach Suggests Unbalanced Proteasome Functioning Induced by the Growth-Promoting Bacterium Kosakonia radicincitans in Arabidopsis | Plant Science | Plant-microbe interaction | Scoop.it
Endophytic plant growth-promoting bacteria have significant impact on the plant physiology and understanding this interaction at the molecular level is of particular interest to support crop productivity and sustainable production systems. We used a proteomics approach to investigate the molecular mechanisms underlying plant growth promotion in the interaction of Kosakonia radicincitans DSM 16656 with Arabidopsis thaliana. Four weeks after the inoculation, the proteome of roots from inoculated and control plants was compared using two-dimensional gel electrophoresis and differentially abundant protein spots were identified by liquid chromatography tandem mass spectrometry. Twelve protein spots were responsive to the inoculation, with the majority of them being related to cellular stress reactions. The protein expression of 20S proteasome alpha-3 subunit was increased by the presence of K. radicincitans. Determination of proteasome activity and immuno blotting analysis for ubiquitinated proteins revealed that endophytic colonisation interferes with ubiquitin-dependent protein degradation. Inoculation of rpn12a, defective in a 26S proteasome regulatory particle, enhanced the growth-promoting effect. This indicates that the plant proteasome, besides being a known target for plant pathogenic bacteria, is involved in the establishment of beneficial interactions of microorganisms with plants.
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Arabidopsis leucine-rich repeat receptor–like kinase NILR1 is required for induction of innate immunity to parasitic nematodes

Arabidopsis leucine-rich repeat receptor–like kinase NILR1 is required for induction of innate immunity to parasitic nematodes | Plant-microbe interaction | Scoop.it
Plant-parasitic nematodes are destructive pests causing losses of billions of dollars annually. An effective plant defence against pathogens relies on the recognition of pathogen-associated molecular patterns (PAMPs) by surface-localised receptors leading to the activation of PAMP-triggered immunity (PTI). Extensive studies have been conducted to characterise the role of PTI in various models of plant-pathogen interactions. However, far less is known about the role of PTI in roots in general and in plant-nematode interactions in particular. Here we show that nematode-derived proteinaceous elicitor/s is/are capable of inducing PTI in Arabidopsis in a manner dependent on the common immune co-receptor BAK1. Consistent with the role played by BAK1, we identified a leucine-rich repeat receptor-like kinase, termed NILR1 that is specifically regulated upon infection by nematodes. We show that NILR1 is essential for PTI responses initiated by nematodes and nilr1 loss-of-function mutants are hypersusceptible to a broad category of nematodes. To our knowledge, NILR1 is the first example of an immune receptor that is involved in induction of basal immunity (PTI) in plants or in animals in response to nematodes. Manipulation of NILR1 will provide new options for nematode control in crop plants in future.
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SINAT E3 Ligases Control the Light-Mediated Stability of the Brassinosteroid-Activated Transcription Factor BES1 in Arabidopsis

SINAT E3 Ligases Control the Light-Mediated Stability of the Brassinosteroid-Activated Transcription Factor BES1 in Arabidopsis | Plant-microbe interaction | Scoop.it
The plant hormones brassinosteroids (BRs) participate in light-mediated regulation of plant growth, although the underlying mechanisms are far from being fully understood. In addition, the function of the core transcription factor in the BR signaling pathway, BRI1-EMS-SUPPRESSOR 1 (BES1), largely depends on its phosphorylation status and its protein stability, but the regulation of BES1 is not well understood. Here, we report that SINA of Arabidopsis thaliana (SINATs) specifically interact with dephosphorylated BES1 and mediate its ubiquitination and degradation. Our genetic data demonstrated that SINATs inhibit BR signaling in a BES1-dependent manner. Interestingly, we found that the protein levels of SINATs were decreased in the dark and increased in the light, which changed BES1 protein levels accordingly. Thus, our study not only uncovered a new mechanism of BES1 degradation but also provides significant insights into how light conditionally regulates plant growth through controlling accumulation of different forms of BES1.
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Ten simple rules for considering preprints

So why make your work available as preprints? There are perceived positives and negatives to disclosing scientific work in the form of a preprint, explored here in the form of 10 Simple Rules. These rules, if they pass review, will appear as part of the PLOS Computational Biology Ten Simple Rules Collection. The rules cover such issues as reward, incentives, speed of dissemination, quality, scooping, and record of priority. You cannot have an article describing preprints, without itself being a preprint!!
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Bodyguards: Pathogen-Derived Decoys That Protect Virulence Factors

Bodyguards: Pathogen-Derived Decoys That Protect Virulence Factors | Plant-microbe interaction | Scoop.it
Recent studies on plant-pathogen interactions have exposed a new strategy used by plant pathogens: decoy effectors that protect virulence factors. Examples of these “bodyguards” include the recently discovered PsXLP1 from Phytophthora sojae and truncated TALEs from Xanthomonas oryzae. These examples suggest important roles for seemingly non-functional effector proteins in distracting the host.
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