Biology subjects

Lechner, E.

Publications and source records attributed to Lechner, E..

5 recordsLinked to original sources

bioRxiv2026

Cessation of diel vertical migration by an inshore dinoflagellate bloom under prey deprivation

Many dinoflagellates are mixotrophic and regulate their vertical position to navigate dynamic gradients in light, nutrients, and prey. Here, it is shown that the obligate kleptoplastidic mixotroph, Dinophysis acuminata, transitions from diel vertical migration to formation of a stationary, sub-surface thin layer in response to prolonged prey deprivation. An inshore bloom within a salt marsh kettle pond was recorded through continuous in-situ imaging, automated oxygen and fluorescence depth profiling, and targeted water chemistry measurements. During the blooms initial development, D. acuminata cells were photosynthetically active and divided vegetatively while vertically migrating. As photosynthesis and growth slowed, vertical migration ceased and cells formed a stable thin layer that promoted conditions for local acidification and nitrogen remineralization. Surface avoidance by the thin layer drove selective retention of cells within the relatively deep kettle hole. Together, these findings illustrate linkage of metabolic state and swimming behavior in D. acuminata and show how swimming behavior can drive development of toxic blooms within inshore systems. They also illustrate how D. acuminata and other eurytolerant bloom-forming species can exploit and shape physicochemical gradients associated with coastal eutrophication.

ecology↗

bioRxiv2024

Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral-induced cellular damage

AbstractRNA viruses co-opt the host endomembrane system and organelles to build replication complexes for infection. How the host responds to these membrane perturbations is poorly understood. Here, we explore the autophagic response of Arabidopsis thaliana to three viruses that hijack different cellular compartments. Autophagy is significantly induced within systemically infected tissues, its disruption rendering plants highly sensitive to infection. Contrary to being an antiviral defense mechanism as previously suggested, quantitative analyses of the viral loads established autophagy as a tolerance pathway. Further analysis of one of these viruses, the Turnip Crinkle Virus (TCV) that hijack mitochondria, showed that despite perturbing mitochondrial integrity, TCV does not trigger a typical mitophagy response. Instead, TCV and Turnip yellow mosaic virus (TYMV) infection activates a distinct selective autophagy mechanism, where oligomeric metabolic enzymes moonlight as selective autophagy receptors and degrade key executors of defense and cell death such as EDS1. Altogether, our study reveals an autophagy-regulated metabolic rheostat that gauges cellular integrity during viral infection and degrades cell death executors to avoid catastrophic amplification of immune signaling.

plant biology↗

bioRxiv2023

Arabidopsis AGO1 N-terminal Poly-Q domain promotes phase separation and association with stress granules during heat stress

In Arabidopsis thaliana, ARGONAUTE1 (AGO1) plays a central role in microRNA (miRNA) and small interfering RNA (siRNA)-mediated silencing. Nuclear AGO1 is loaded with miRNAs and exported to the cytosol where it associates to the rough ER to conduct miRNA-mediated translational repression, mRNA cleavage and biogenesis of phased siRNAs. These latter, as well as other cytosolic siRNAs, are loaded into cytosolic AGO1, but in which compartment this happens is not known. Moreover, the effect of stress on AGO1 localization is still unclear. Here, we show that a 37{degrees}C heat stress (HS) promotes AGO1 protein accumulation in cytosolic condensates where it co-localizes with components of siRNA bodies and of stress granules (SGs). AGO1 contains a prion-like domain in its poorly characterized N-terminal Poly-Q domain, which, is sufficient to undergo phase separation, independent of the presence or absence of SGS3. HS only moderately affects the small RNA repertoire, the loading of AGO1 by miRNAs and the signatures of target cleavage, suggesting that its localization in condensates protects AGO1 rather than promotes or impairs its activity in reprograming gene expressing during stress. Collectively, our work shed new light on the impact of high temperature on a main effector of RNA silencing in plants.

plant biology↗

bioRxiv2021

The Arabidopsis F-box protein FBW2 degrades AGO1 to avoid spurious loading of illegitimate small RNA

RNA silencing is a conserved mechanism in eukaryotes and is involved in development, heterochromatin maintenance and defense against viruses. In plants, ARGONAUTE1 (AGO1) protein plays a central role in both microRNA (miRNA) and small interfering RNA (siRNA)-directed silencing and its expression is regulated at multiple levels. Here, we report that the F-box protein FBW2 targets proteolysis of AGO1 by a CDC48-mediated mechanism. We found that FBW2 assembles an SCF complex that recognizes the MID-PIWI domain of AGO1 and requires its C-terminal domain containing a GW motif for AGO1 turnover. We showed that FBW2 prefers the unloaded and some mutated forms of AGO1 protein. While FBW2 loss of function does not lead to strong growth or developmental defects, it significantly increases RNA silencing activity. Interestingly, under conditions in which small RNA production or accumulation is affected, the failure to degrade AGO1 in fbw2 mutants becomes more deleterious for the plant. Hence, the non-degradable AGO1 protein assembles high molecular weight complexes and binds illegitimate small RNA leading to the cleavage of new target genes that belong to stress responses and cellular metabolic processes. Therefore, the control of AGO1 homeostasis by ubiquitin ligases plays an important role in quality control to avoid off-target cleavage.

cell biology↗

bioRxiv2021

Molecular features of RNA silencing against phloem-restricted polerovirus TuYV enable amplification of silencing signal from host transcripts

In plants and some animal lineages, RNA silencing is an efficient and adaptable defense mechanism against viruses. To counter it, viruses encode suppressor proteins that interfere with RNA silencing. Phloem-restricted viruses are spreading at an alarming rate and cause substantial reduction of crop yield, but how they interact with their hosts at the molecular level is still insufficiently understood. Here, we investigate the antiviral response against phloem-restricted turnip yellows virus (TuYV) in the model plant Arabidopsis thaliana. Using a combination of genetics, deep sequencing, and mechanical vasculature enrichment, we show that the main axis of silencing active against TuYV involves 22-nt vsiRNA production by DCL2, and their preferential loading into AGO1. Unexpectedly, and despite the viral encoded VSR P0 previously shown to mediate degradation of AGO proteins, vascular AGO1 undergoes specific post-translational stabilization during TuYV infection. We also identify vascular novel secondary siRNA produced from conserved plant transcripts and initiated by DCL2-processed AGO1-loaded vsiRNA, supporting a viral strategy to modulate host response. Collectively, our work uncovers the complexity of antiviral RNA silencing against phloem-restricted TuYV and prompts a re-assessment of the role of its suppressor of silencing P0 during genuine infection.

plant biology↗