Biology subjects

Hafren, A.

Publications and source records attributed to Hafren, A..

8 recordsLinked to original sources

bioRxiv2025

Effector-triggered processing body formation attenuates host translation via ER stress responses and autophagy upon bacterial infection

Pathogens employ sophisticated strategies to modulate host protein homeostasis by targeting proteolytic pathways, but their impact on protein synthesis remains elusive. We report that pathogenic bacteria Pseudomonas syringae (Pst) targets ribonucleoprotein condensates, known as processing bodies (P-bodies), to attenuate host translation through two effectors with liquid-like properties. We uncovered a previously unknown link that Pst-mediated repression of the ER stress response is required for P-body assembly. Furthermore, we identify a novel intersection between P-bodies and autophagy, demonstrating that autophagic clearance of P-bodies is crucial for maintaining the balance between translationally active and inactive mRNAs. Altogether, our discoveries provide novel insights on how host translation is attenuated by bacteria to dampen plant immunity and uncover unknown connections between ER stress responses and autophagy with P-body dynamics.

plant biology↗

bioRxiv2022

Cauliflower mosaic virus disease spectrum uncovers novel susceptibility factor NCED9 in Arabidopsis thaliana

Viruses are intimately linked with their hosts and especially dependent on gene-for-gene interactions to establish successful infections. The genotype of their hosts thus has a strong influence on the outcome virus disease. On the host side, defence mechanisms like tolerance and resistance can occur within the same species leading to differing virus accumulation in relation to symptomology and plant fitness. The identification of novel resistance genes and susceptibility factors against viruses is an important part in understanding viral pathogenesis and securing food production. The model plant Arabidopsis thaliana displays a wide symptom spectrum in response to RNA virus infections and unbiased genome-wide association studies have proven a powerful tool to identify novel disease-genes. In this study we infected natural accessions of Arabidopsis thaliana with the pararetrovirus Cauliflower mosaic virus to study the phenotypic variations between accessions and their correlation with virus accumulation. Through genome-wide association mapping of viral accumulation differences, we identified several susceptibility factors for CaMV, the strongest of which was the abscisic acid synthesis gene NCED9. Further experiments confirmed the importance of abscisic acid homeostasis and its disruption for CaMV disease.

plant biology↗

bioRxiv2022

Cauliflower mosaic virus protein P6 forms a microenvironment for RNA granule proteins and interferes with stress granule responses

Biomolecular condensation is a multipurpose cellular process that viruses use ubiquitously in their multiplication. CaMV replication complexes are condensates that differ from most viruses in being non-membranous assemblies and consist of RNA and protein, mainly viral protein P6. Despite description of these viral factories already half a century ago with many observations that followed since, functional details of the condensation process, their properties and relevance has remained enigmatic. Our main findings include a large dynamic mobility range of host proteins within viral factories, while the viral matrix protein P6 is immobile in accordance with representing the central node of these condensates. As novel components of VFs we identify stress granule (SG) nucleating factors G3BP7 and the UBP1 family. Similarly, as SG components localize in VFs during infection, ectopic P6 localizes to SGs and reduces their assembly after stress. Intriguingly, it appears that soluble rather than condensed P6 suppresses SGs and mediates also other essential P6 functions, suggesting that the increased condensation over the infection time-course may accompany a progressive shift in selected P6 functions. Together, this study highlights VFs as dynamic condensates and P6 as a complex modulator of SG responses.

plant biology↗

bioRxiv2021

Cauliflower Mosaic Virus Utilizes Processing Bodies to Escape Translational Repression in Arabidopsis

Viral infections impose extraordinary RNA stress on a cell, triggering cellular RNA surveillance pathways like RNA decapping, nonsense-mediated decay and RNA silencing. Viruses need to maneuver between these pathways to establish infection and succeed in producing high amounts of viral proteins. Processing bodies (PBs) are integral to RNA triage in eukaryotic cells with several distinct RNA quality control pathways converging for selective RNA regulation. In this study, we investigate the role of Arabidopsis thaliana PBs during Cauliflower Mosaic Virus (CaMV) infection. We find that several PB components are co-opted into viral replication factories and support virus multiplication. This pro-viral role was not associated with RNA decay pathways but instead, we could establish PB components as essential helpers in viral RNA translation. While CaMV is normally resilient to RNA silencing, PB dysfunctions expose the virus to this pathway, similar to previous observations on transgenes. Transgenes, however, undergo RNA Quality Control dependent RNA degradation, whereas CaMV RNA remains stable but becomes translationally repressed through decreased ribosome association, revealing a unique dependence between PBs, RNA silencing and translational repression. Together, our study shows that PB components are co-opted by the virus to maintain efficient translation, a mechanism not associated with canonical PB functions.

plant biology↗

bioRxiv2021

Turnip crinkle virus targets host ATG8 proteins to attenuate antiviral autophagy

Autophagy has emerged as a central player in plant virus disease and resistance. In this study we have addressed the potential roles of autophagy in Turnip crinkle virus (TCV) infection. We found that autophagy attenuates disease severity and contributes to resistance against TCV by limiting virus accumulation. These autophagy-dependent disease phenotypes intensify further when combined with defects in RNA silencing, suggesting that these two major defence pathways are largely uncoupled in TCV disease. Intriguingly, as a counterdefence, TCV employs the viral silencing suppressor protein P38 to suppress antiviral autophagy, likely by directly sequestering ATG8 proteins. This strategy appears to be novel for plant viruses, yet resembles mechanisms described for other pathogen classes. Together, these results broaden our understanding of autophagy in plant virus disease, and strengthens our view of virus-specific adaptation to the autophagy pathway.

plant biology↗

bioRxiv2021

Proteasome homeostasis is essential for a robust cauliflower mosaic virus infection

The ubiquitin-proteasome system (UPS) is essential for the maintenance and shifts in protein homeostasis, and thereby forms a founding pillar in virtually all cellular processes including plant immunity and viral infections. According to its importance in fine-tuning the complex plant immune response, proteasomal defects result in divergent outcomes including both resistance and susceptibility phenotypes in response to viruses. The final outcome will largely depend on the specific virus and its specific co-adaptation with the UPS as well as the immune system. Here, we show that cauliflower mosaic virus (CaMV) relies on the proteasome for robust infection. The proteasome system is induced during infection via SA and supports systemic accumulation of the virus as well as plant growth performance during infection. This establishes the UPS as a win-win pathway for the plant and the virus, and together with our demonstration of a proteasome-suppressing viral effector, the intimacy between the proteasome and CaMV is fortified.

plant biology↗

bioRxiv2021

Self-ubiquitination of a pathogen type-III effector traps and blocks the autophagy machinery to promote disease

Beyond its role in cellular homeostasis, autophagy plays anti- and pro-microbial roles in host-microbe interactions, both in animals and plants. One prominent role of anti-microbial autophagy is to degrade intracellular pathogens or microbial molecules, in a process termed xenophagy. Consequently, microbes evolved mechanisms to hijack or modulate autophagy to escape elimination. Although well-described in animals, the extent to which xenophagy contributes to plant-bacteria interactions remains unknown. Here, we provide evidence that Xanthomonas campestris pv. vesicatoria (Xcv) suppresses host autophagy by utilizing type-III effector XopL. XopL interacts with and degrades the autophagy component SH3P2 via its E3 ligase activity to promote infection. Intriguingly, XopL is targeted for degradation by defense-related selective autophagy mediated by NBR1/Joka2, revealing a complex antagonistic interplay between XopL and the host autophagy machinery. Our results implicate plant antimicrobial autophagy in depletion of a bacterial virulence factor and unravels an unprecedented pathogen strategy to counteract defense-related autophagy.

plant biology↗

bioRxiv2020

Autophagic degradation of the Cucumber mosaic virus virulence factor 2b balances antiviral RNA silencing with proviral plant fitness and virus seed transmission

Autophagy is a conserved intracellular degradation pathway that has recently emerged as an integral part of plant responses to virus infection. The elucidated mechanisms of autophagy range from the selective degradation of viral components to a more general attenuation of disease symptoms. In addition, several viruses are able to manipulate the autophagy machinery and counteract autophagy-dependent resistance. Despite these findings, the complex interplay of autophagy activities, viral pathogenicity factors, and host defence pathways in disease development remains poorly understood. In the current study, we analysed the interaction between autophagy and Cucumber mosaic virus (CMV) in Arabidopsis thaliana. We show that autophagy is induced during CMV infection and promotes the turnover of the major CMV virulence protein and RNA silencing suppressor 2b. Intriguingly, 2b itself dampens plant autophagy. In accordance with 2b degradation, we found that autophagy provides resistance against CMV by reducing viral RNA accumulation in an RNA silencing-dependent manner. Moreover, autophagy and RNA silencing pathways contribute to plant longevity and fecundity of CMV infected plants in an additive manner, uncoupling it from resistance. In addition to reduced fecundity, autophagy-deficient plants also failed to support seed transmission of the virus. We propose that autophagy attenuates CMV virulence via 2b degradation and thereby increases both plant and virus fitness with a trade-off penalty arising from increased RNA silencing-mediated resistance. Author summaryThe capacity of plants to fight pathogenic viruses in order to survive and minimize damage relies on profound cellular reprogramming events. These include the synthesis of new as well as the degradation of pre-existing cellular components, together shifting cellular homeostasis towards a better tolerance of disease and fortification of antiviral defence mechanisms. Autophagy is a prominent and highly conserved cellular degradation pathway that supports plant stress resilience. Autophagy functions vary broadly and range from rather unspecific renewal of cytoplasm to highly selective degradation of a wide collection of specific substrates. Autophagy is well established to be involved during virus infections in animals, and its importance has also recently emerged in virus diseases of plants. However, we are still far from a comprehensive understanding of the complexity of autophagy activities in host-virus interactions and how autophagy pathway engineering could be applied against viruses. Here, we have analyzed one of the traditional model plant viruses, Cucumber mosaic virus (CMV), and its interactions with autophagy. Our study revealed that autophagy is tightly integrated into CMV disease, influencing processes from plant health to CMV epidemiology.

plant biology↗