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Kilian, J.

Publications and source records attributed to Kilian, J..

8 recordsLinked to original sources

Pre-chlorotic Mg2+ deficiency impairs guard-cell PSII and leaf gas exchange in Vicia faba

Magnesium deficiency impairs photosynthesis and transpiration before visible chlorosis, but whether guard cells themselves are affected at this early stage remains unresolved. We combined whole-leaf gas exchange and chlorophyll fluorescence with cell-specific fluorescence measurements of individual guard cell pairs, together with elemental analysis, metabolite profiling, adenosine triphosphate quantification, and proteome profiling of guard cell-enriched material in hydroponically grown Vicia faba. Magnesium deficiency reduced magnesium concentrations in both whole leaves and guard cell-enriched fractions. Under red light, magnesium-deficient leaves showed reduced effective quantum yield of photosystem II, CO2 assimilation, transpiration, and stomatal conductance, whereas intercellular CO2 concentration remained unchanged. Individual guard cell pairs likewise showed reduced effective quantum yield of photosystem II, demonstrating that the early deficiency response extended to guard cells. Electron transport rate and non-photochemical quenching in guard cells were not significantly altered. Only a small set of metabolites in guard cell-enriched material, mainly fatty acids and citrate, responded to magnesium deficiency, whereas ATP abundance and light-induced proton extrusion remained unchanged. In contrast, the guard cell-enriched proteome showed higher abundance of photosynthesis- and translation-related proteins despite reduced guard-cell PSII efficiency. Together, these findings identify guard cells as an early responsive cell type under magnesium deficiency and show that guard-cell photochemistry is impaired before visible chlorosis, alongside reduced whole-leaf carbon gain and water loss.

physiology↗

Resistance Training Reshapes the Gut Microbiome for Better Health

ObjectivesThe gut microbiome plays a critical role in metabolism, immunity, and aging. While endurance training has been shown to beneficially modulate the microbiome, the effects of resistance training remain less clear, with some studies reporting minimal changes. This project aims to investigate whether structured resistance training elicits significant changes in gut microbiome composition and diversity in sedentary, healthy adults. Methods150 participants completed an 8-week supervised resistance training program. Session-level training data, including weights and repetitions, were recorded alongside metrics like load and compliance. Fecal samples were collected throughout the study period at designated timepoints for 16S rRNA gene amplicon sequencing to assess microbiome composition and for metabolomics analyses to evaluate microbial metabolic activity. ResultsNo differences in microbial diversity were observed, and there were no significant changes in microbial community composition or fecal metabolomics across all participants post-training. However, within-individual microbial community changes significantly correlated with strength improvement, and significantly stronger shifts in beta diversity were observed in participants with high average strength gains compared to those with smaller gains. In these high responders, differential abundance analysis revealed time-dependent microbial changes, with more taxa enriched or depleted by week 8 of training. Notably, Faecalibacterium and Roseburia hominis--both associated with a healthier, anti-inflammatory microbiome--were significantly enriched. Many differentially abundant taxa belonged to the Lachnospiraceae family. ConclusionResistance training drives significant, time-dependent gut microbiome changes, particularly in those demonstrating greater improvements in strength. These shifts mirror endurance training effects and may reflect improved overall health. SummaryWhile endurance training has been consistently shown to enhance gut microbiome composition, the effects of resistance training remain less well defined, with findings to date being variable. Our results indicate that resistance training can induce meaningful, time-dependent shifts in the gut microbiome, particularly among sedentary individuals who experience substantial strength gains. Notably, we observed enrichment of key health-associated taxa, including Faecalibacterium and Roseburia hominis, both linked to anti-inflammatory effects and improved gut function. These findings suggest that resistance training may contribute to gut health in conjunction with physical fitness, supporting its broader application in health promotion strategies and future microbiome-focused research.

microbiology↗

Emergent loss of microbial biodiversity with increasing resource diversity

The origin of biodiversity is arguably the most fundamental question in ecology -- especially how countless microbial species coexist within a single community. A prevailing hypothesis holds that microbial species coexist by specializing on different resources, thereby reducing competition. Accordingly, increasing resource diversity is expected to promote species coexistence and boost biodiversity. Surprisingly, we observe the opposite: microbial biodiversity often declines as resource diversity increases. This unexpected result emerges from a widespread physiological response across diverse microbial taxa, in which more complex environments trigger higher overall resource uptake. This intensifies competition and drives biodiversity loss. Updating a central ecological model to include this physiological trait accurately reproduces the observed decline. Our findings demonstrate that physiological changes at the individual level can overturn classical ecological principles and scale up to restructure entire ecosystems.

microbiology↗

MYB68 orchestrates cork differentiation by regulating stem cell proliferation and suberin deposition

Plants have developed specialized barriers to protect and isolate the inner tissues from the environment while maintaining homeostasis. Different barriers are present in various organs and at different growth stages. During secondary growth, the periderm acts as the protective tissue, covering roots, stems, and branches as they become thick. The periderm is a dynamic barrier comprising a stem cell niche known as the cork cambium, which bifacially divides to generate the phelloderm inward and the cork outward. Cork cells have a unique cell wall impregnated with suberin and lignin polymers, essential for the barrier function. Despite its importance, the differentiation process that forms new cork cells from the stem cell is largely unknown. In this work, we identify members of the MYB36-subclade transcription factors as key regulators of cork differentiation. On the one hand, this set of transcription factors promotes suberin deposition by inducing the expression of enzymes involved in all steps of suberin biosynthesis, including the recently discovered suberin-polymerizing enzymes GDS Lipases; on the other hand, it represses cork cambium proliferation. Furthermore, we demonstrated that suberin deposition in the cork is a robust process regulated by a complex network of transcription factors, including other MYB transcription factors that activate suberin deposition in the endodermis. However, only members of the MYB36 subclade can repress cell proliferation in different developmental contexts, highlighting general and specific functions for MYB transcription factors. These findings have broad applicability, as tissue-specific manipulation of MYB activity has the potential for improving traits of biotechnological interest, such as thicker periderms and more suberized cork layers, and for assessing how these traits affect plant performance in response to stresses.

plant biology↗

The genetic interaction of REVOLUTA and WRKY53 links plant development, senescence, and immune responses

In annual plants, tight coordination of successive developmental events is of primary importance to optimize performance under fluctuating environmental conditions. The recent finding of the genetic interaction of WRKY53, a key senescence-related gene with REVOLUTA, a master regulator of early leaf patterning, raises the question of how early and late developmental events are connected. Here, we investigated the developmental and metabolic consequences of an alteration of the REVOLUTA and WRKY53 gene expression, from seedling to fruiting. Our results show that REVOLUTA critically controls late developmental phases and reproduction while inversely WRKY53 determines vegetative growth at early developmental stages. We further show that these regulators of distinct developmental phases frequently, but not continuously, interact throughout ontogeny and demonstrated that their genetic interaction is mediated by the salicylic acid (SA). Moreover, we showed that REVOLUTA and WRKY53 are keys regulatory nodes of development and plant immunity thought their role in SA metabolic pathways, which also highlights the role of REV in pathogen defence. Together, our findings demonstrate how late and early developmental events are tightly intertwined by molecular hubs. These hubs interact with each other throughout ontogeny, and participate to the interplay between plant development and immunity.

plant biology↗

5-Deoxyadenosine Salvage by Promiscuous Enzyme Activity leads to Bioactive Deoxy-Sugar Synthesis in Synechococcus elongatus

7-Deoxysedoheptulose is an unusual deoxy-sugar, which acts as antimetabolite of the shikimate pathway thereby exhibiting antimicrobial and herbicidal activity. It is produced by the unicellular cyanobacterium Synechococcus elongatus PCC 7942, which has a small, stream-lined genome, assumed to be free from gene clusters for secondary metabolite synthesis. In this study, we identified the pathway for the synthesis of 7-deoxysedoheptulose. It originates from 5-deoxyadenosine, a toxic byproduct of radical S-adenosylmethionine (SAM) enzymes, present in all domains of life. Thereby we identified a novel 5-deoxyadenosine salvage pathway, which first leads to the synthesis and excretion of 5-deoxyribose and subsequently of 7-deoxysedoheptulose. Remarkably, all reaction steps are conducted by promiscuous enzymes. This is a unique example for the synthesis of a bioactive compound without involving a specific gene cluster. This challenges the view on bioactive molecule synthesis by extending the range of possible compounds beyond the options predicted from secondary metabolite gene clusters.

biochemistry↗

Tissue-autonomous phenylpropanoid production is essential for establishment of root barriers

Plants deposit polymeric barriers in their root cell walls to protect against external stress and facilitate selective nutrient uptake. The compounds that make up these barriers originate from the fatty acid- and phenylpropanoid biosynthetic pathways. Although the machinery responsible for production of the barrier constituents is well-char-acterized, our pathway models lack spatiotemporal resolution - especially in roots - and the source tissue is often not clear due to the apoplastic nature of barriers. Insights into how the individual root tissues or cells contribute to forming apoplastic barriers is important for elucidation of their ultrastructure, function and development. Manipulation of the associated biosynthesis is delicate, as mutants often display pleiotropic phenotypes due to the broad role of the underlying metabolites. Here, we address these issues by creating a genetic tool that allows in vivo repression of the phenylpropanoid pathway with both spatial and temporal control. We provide strong evidence that tissue-auton-omous production of phenylpropanoids is essential for establishment of the endodermal Casparian strip. Moreover, we find that in order to maintain deposition and attachment of a coherent suberin matrix to the cell wall, cells require continuous production of aromatic constituents. This process is especially crucial in the suberized endodermis where we find that repression of phenylpropanoid production leads to active removal of suberin.

plant biology↗

The BIR2/BIR3-interacting Phospholipase D gamma 1 negatively regulates immunity in Arabidopsis

Plants have evolved effective strategies to defend themselves against pathogen invasion. Starting from the plasma membrane with the recognition of microbe-associated molecular patterns (MAMPs) via pattern recognition receptors, internal cellular signaling pathways are induced to ultimately fend off the attack. Phospholipase D (PLD) hydrolyzes membrane phospholipids to produce phosphatidic acid (PA), which has been proposed to play a second messenger role in immunity. The Arabidopsis PLD family consists of 12 members and for some a specific function in resistance towards a subset of pathogens has been shown. We demonstrate here that Arabidopsis PLD{gamma}1, but not its close homologs PLD{gamma}2 and PLD{gamma}3, is specifically involved in plant immunity. Genetic inactivation of PLD{gamma}1 resulted in increased resistance towards the virulent bacterium Pseudomonas syringae pv. tomato DC3000 and the necrotrophic fungus Botrytis cinerea. As pld{gamma}1 mutant plants responded with elevated levels of reactive oxygen species to MAMP-treatment, a negative regulatory function for this PLD isoform is proposed. Importantly, PA levels in pld{gamma}1 mutants were not affected compared to stressed wild-type plants, suggesting that alterations in PA levels are unlikely the cause for the enhanced immunity in the pld{gamma}1 line. Instead, the plasma-membrane-attached PLD{gamma}1 protein colocalized and associated with the receptor-like kinases BIR2 and BIR3, which are known negative regulators of pattern-triggered immunity. Moreover, complex formation of PLD{gamma}1 and BIR2 was further promoted upon MAMP-treatment. Hence, we propose that PLD{gamma}1 acts as a negative regulator of plant immune responses in complex with immunity-related proteins BIR2 and BIR3.\n\nOne-sentence summaryA phospholipase D is a novel negative regulator of plant immunity and forms complexes with regulatory receptor-like kinases.

plant biology↗