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Eschen-Lippold, L.

Publications and source records attributed to Eschen-Lippold, L..

6 recordsLinked to original sources

Fungal community composition links rhizosphere microbiome organization to plant phenotype in response to moderate warming

BackgroundGlobal warming increasingly challenges plant performance and ecosystem function, and plant responses to elevated temperature are shaped not only by intrinsic plasticity, but also by interactions with rhizosphere microbial communities. However, it remains unclear how warming-induced microbiome reorganization relates to plant performance, whether microbiome community composition predicts plant phenotypic responses to elevated temperature better than simple host-microbiome origin matching, and which bacterial or fungal community features contribute most strongly to this prediction. ResultsWe implemented a full factorial design manipulating plant genotype (P), microbial inoculum (M), and temperature (T) using natural Arabidopsis thaliana ecotypes and their corresponding rhizosphere microbiomes from contrasting climatic regions. By integrating high-throughput plant phenotyping, microbial community profiling, microbiome-phenotype coupling analyses, and predictive modeling, we found that elevated temperature induced a coherent thermomorphogenic shift in plant architecture, while plant phenotypic variation remained determined primarily by genotype over the 14-day vegetative growth period covered in this study. Overall, cold-origin genotypes showed larger temperature-induced trait shifts than warm-origin genotypes. Rhizosphere microbial communities were structured predominantly by inoculum origin, but were also affected by warming. Evidence for a increased thermomorphogenic growth when genotypes were combined with inoculum from their home site was limited. Instead, microbiome-phenotype associations were better captured by community composition than by matching status, with fungal community variation showing stronger and more consistent associations with plant phenotype than bacterial variation and providing more robust predictions of plant phenotypes across models. ConclusionsWarming reorganized plant-rhizosphere systems within persistent host- and inoculum-associated baselines. Plant phenotypic variation during vegetative development under elevated temperature was linked more closely to microbiome composition, especially in fungi, than to simple host-microbiome matching of origins. These findings provide a framework for identifying microbiome features associated with plant performance under climate warming.

plant biology↗

Auxin-dependent acceleration of cell division rates regulates root growth at elevated temperature

Roots are highly plastic organs enabling plants to acclimate to a changing below-ground environment. In addition to abiotic factors like nutrients or mechanical resistance, plant roots also respond to temperature variation. Below the heat stress threshold, Arabidopsis thaliana seedlings react to elevated temperature by promoting primary root growth, possibly to reach deeper soil regions with potentially better water saturation. While above-ground thermomorphogenesis is enabled by thermo-sensitive cell elongation, it was unknown how temperature modulates root growth. We here show that roots are able to sense and respond to elevated temperature independent of shoot-derived signals. A yet unknown root thermosensor seems to employ auxin as a messenger to promote primary root growth. Growth is primarily achieved by accelerating cell division rates in the root apical meristem, likely maintained via temperature-sensitive organization of the polar auxin transport system. Hence, the primary cellular target of elevated ambient temperature differs fundamentally between root and shoot tissues, while the messenger auxin that relays temperature information to elongating or dividing cells, respectively, remains the same.

plant biology↗

Differential requirement for the EDS1 catalytic triad in A. thaliana and N. benthamiana

O_LIHeterodimeric complexes incorporating the lipase-like proteins EDS1 with PAD4 or SAG101 are central hubs in plant innate immunity. EDS1 functions encompass signal relay from TIR domain-containing intracellular NLR-type immune receptors (TNLs) towards RPW8-type helper NLRs (RNLs) and, in A. thaliana, bolstering of signaling and resistance mediated by cell-surface pattern recognition receptors (PRRs). Biochemical activities underlying these mechanistic frameworks remain unknown. C_LIO_LIWe used CRISPR/Cas-generated mutant lines and agroinfiltration-based complementation assays to interrogate functions of EDS1 complexes in N. benthamiana. C_LIO_LIWe do not detect impaired PRR signaling in N. benthamiana lines deficient in EDS1 complexes or RNLs. Intriguingly, mutations within the catalytic triad of Solanaceae EDS1 can abolish or enhance TNL immunity in N. benthamiana. Furthermore, nuclear EDS1 accumulation is sufficient for N. benthamiana TNL (Roq1) immunity. C_LIO_LIReinforcing PRR signaling in Arabidopsis might be a derived function of the TNL/EDS1 immune sector. Dependency of Solanaceae but not A. thaliana EDS1 on catalytic triad residues raises the possibility that a TNL-derived small molecule binds to the Solanaceae EDS1 lipase-like domain, and that EDS1 lipase-like domain pocket contributions to TNL immune responses vary between lineages. Whether and how nuclear EDS1 activity connects to membrane pore-forming RNLs remains unknown. C_LI

plant biology↗

Dosage of duplicated and antifunctionalized homeobox proteins influences spikelet development in barley

Illuminating the mechanisms of inflorescence architecture of grain crops that feed our world may strengthen the goal towards sustainable agriculture. Lateral spikelet development of barley (Hordeum vulgare L.) is such an example of a floral architectural trait regulated by VRS1 (Vulgare Row-type Spike 1 or Six-rowed Spike 1, syn. HvHOX1). Its lateral spikelet-specific expression and the quantitative nature of suppressing spikelet development were previously shown in barley. However, the mechanistic function of this gene and its paralog HvHOX2 on spikelet development is still fragmentary.Here, we show that these duplicated transcription factors (TFs) have contrasting nucleotide diversity in various barley genotypes and several Hordeum species. Despite this difference, both proteins retain their basic properties of the homeodomain leucine zipper class I family of TFs. During spikelet development, these genes exhibit similar spatiotemporal expression patterns yet with anticyclic expression levels. A gene co-expression network analysis suggested that both have an ancestral relationship but their functions appear antagonistic to each other, i.e., HvHOX1 suppresses whereas HvHOX2 rather promotes spikelet development. Our transgenic promoter-swap analysis showed that HvHOX2 can restore suppressed lateral spikelets when expression levels are increased; however, at its low endogenous expression level, HvHOX2 appears dispensable for spikelet development. Collectively, this study proposes that the dosage of the two antagonistic TFs, HvHOX1 and HvHOX2, influence spikelet development in barley.

plant biology↗

Differential N-end rule degradation of RIN4/NOI fragments generated by the AvrRpt2 effector protease

The protein RPM1-INTERACTING PROTEIN4 (RIN4) is a central regulator of both layers of plant immunity systems, the so-called pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). RIN4 is targeted by several effectors, including the Pseudomonas syringae protease effector AvrRpt2. Cleavage of RIN4 by AvrRpt2 generates unstable RIN4 fragments, whose degradation leads to the activation of the resistance protein RPS2 (RESISTANT TO P. SYRINGAE2). Hence, identifying the determinants of RIN4 degradation is key to understanding RPS2-mediated ETI, as well as virulence functions of AvrRpt2. In addition to RIN4, AvrRpt2 cleaves host proteins from the nitrate-induced (NOI) domain family. Although cleavage of NOI-domain proteins by AvrRpt2 may contribute to PTI regulation, the (in)stability of these proteolytic fragments and the determinants that regulate their stability have not been examined. Notably, a common feature of RIN4 and of many NOI-domain protein fragments generated by AvrRpt2 cleavage is the exposure of a new N-terminal residue that is destabilizing according to the N-end rule. Using antibodies raised against endogenous RIN4, we show that the destabilization of AvrRpt2-cleaved RIN4 fragments is independent of the N-end rule pathway (recently renamed N-degron pathway). By contrast, several NOI-domain protein fragments are bona fide substrates of the N-degron pathway. The discovery of this novel set of substrates considerably expands the number of proteins targeted for degradation by this ubiquitin-dependent pathway, for which very few physiological substrates are known in plants. Our results also open new avenues of research to understand the role of AvrRpt2 in promoting bacterial virulence.\n\nOne sentence summaryAnalysis of RIN4/NOI fragments released after cleavage by the bacterial effector protease AvrRpt2 reveals a novel role of the N-end rule in the degradation of NOI-domain proteins, but not of RIN4.

plant biology↗

Phosphorylation of the exocyst subunit Exo70B2 contributes to the regulation of its function

The exocyst is a conserved hetero-octameric complex that mediates early tethering of post-Golgi vesicles during exocytosis. Its Exo70 subunit functions as a spatiotemporal regulator by mediating numerous interactions with proteins and lipids. However, a molecular understanding of the exocyst functions remains challenging. Exo70B2 localized to dynamic foci at the plasma membrane and transited through Brefeldin A (BFA)-sensitive compartments, indicating that it participates in conventional secretion. Conversely, treatment with the immunogenic peptide flg22 or the salicylic acid (SA) defence hormone analogue Benzothiadiazole (BTH), induced Exo70B2 transport into the vacuole where it colocalized with autophagic markers AUTOPHAGY-RELATED PROTEIN 8 (ATG8) and NEIGHBOR OF BRCA1 GENE 1 (NBR1). According with its role in immunity, we discovered that Exo70B2 interacts with and is phosphorylated by the MITOGEN-ACTIVATED PROTEIN KINASE 3 (MPK3). Mimicking phosphorylation inhibited Exo70B2 localization at sites of active secretion. By contrast, lines expressing phosphonull variants displayed higher Effector-Triggered Immunity and were hypersensitive to BTH, conditions known to induce the secretory pathway. Our results suggest a molecular mechanism by which phosphorylation of Exo70B2 regulates interaction with the plasma membrane, and couples the secretory pathway with cellular signalling.

cell biology↗