Biology subjects

Zumsteg, J.

Publications and source records attributed to Zumsteg, J..

9 recordsLinked to original sources

bioRxiv2026

Decoupling glycation from mortality: glucose, but not methylglyoxal, reduces survival in zebra finches

Birds provide a unique model for ageing research, with greater longevity and slower senescence compared to mammals of similar body size, despite a higher mass-adjusted metabolic rate and blood glucose levels than other vertebrate groups. While the effects of glucose, glycation, and advanced glycation end-products (AGE) on ageing are well-documented in biomedical research, their impact on avian physiology and ageing remains poorly understood. Although birds may possess adaptations mitigating the potential detrimental effects of glucose, elevated glucose still predicts reduced lifespan, and protein glycation varies with age and can influence survival and some fitness-related traits, implying that glycation or AGE accumulation may have relevant effects on avian longevity. In this study, we experimentally investigated how one year of dietary supplementation with glucose or methylglyoxal affects survival and physiology (metabolic rate, flying performance, and beak coloration) in captive zebra finches (Taeniopygia guttata). We reveal a significant increase in mortality exclusively in glucose-supplemented birds, with also an elevated albumin glycation rate and AGE formation. However, these variables did not directly explain the increased mortality, which was also absent in methylglyoxal-treated individuals, despite similar AGE accumulation. Additionally, we observed some other effects, like an age-related constraint on seasonal metabolic adjustment, a treatment-influenced age decline in secondary sexual traits expression, and a decline in flight performance during the peak mortality period, suggesting a broader deterioration of health. Thus, although we demonstrate glucose supplementation to be more deleterious than methylglyoxal, the underlying mechanisms for the increase in mortality induced by the treatment remain unresolved.

physiology↗

bioRxiv2025

The histone methyltransferase SDG26 shapes cold stress responses in Arabidopsis through chromatin-based regulation of ABA-dependent and ABA-independent pathways

Plants constantly face adverse environmental conditions, including temperature drops that can severely impair growth and productivity. To cope with such stresses, they have evolved complex mechanisms of transcriptional reprogramming. While various cold-responsive pathways have been described, the contribution of chromatin-level regulation, and in particular histone modifications, remains largely obscure. Here, we identify the histone methyltransferase SET DOMAIN GROUP 26 (SDG26) as a positive regulator of cold stress responses in Arabidopsis thaliana. We show that SDG26 is transcriptionally induced and post-transcriptionally stabilized by cold, and that its loss of function leads to increased freezing tolerance but reduced drought tolerance. At the molecular level, SDG26 promotes expression of cold-responsive genes, including members of the CBF-COR regulon, through direct binding and histone H3 lysine 36 trimethylation (H3K36me3) at their chromatin. Concomitantly, SDG26 modulates abscisic acid (ABA) biosynthesis, catabolism, and transport, thereby promoting ABA accumulation, stomatal closure, and drought tolerance. Collectively, our results reveal that SDG26 integrates ABA-dependent and ABA-independent pathways to fine-tune Arabidopsis responses to abiotic stresses. We further establish SDG26 as a chromatin modifier contributing to stress-responsive H3K36me3 enrichment at specific loci. Together, our work identifies SDG26 as a chromatin-based hub balancing cold acclimation with water conservation, thereby enhancing plant resilience.

plant biology↗

bioRxiv2025

Jasmonic Acid Oxidases (JAO) define a new branch in jasmonate metabolism towards 11OH-jasmonic acid and its glucosylated derivative

Jasmonates (JAs) occur in plants as a group of related compounds undergoing complex metabolic conversions that shape signatures unique to a given organ or physiological status. Previous studies have shown that several JAs result from direct or indirect catabolism of the master hormonal regulator jasmonoyl-isoleucine (JA-Ile) that controls most jasmonate responses triggered by developmental or environmental cues. Hydroxylation of the precursor jasmonic acid (JA) by Jasmonic Acid Oxidases (JAO) holds a peculiar regulatory function, by attenuating basal JA-Ile formation and action, and promoting growth. Here we reinvestigated biochemically and genetically the nature and origins of hydroxy-JAs and their derivatives in Arabidopsis. Using refined analytical methods and pathway-impaired mutants, we show that JAO enzymes produce exclusively 11OH-JA and are preferentially recruited in response to fungal infection where 11-O-Glc-JA accumulates as its main glucosylated derivative. In contrast, mechanical wounding triggers the dominant formation of 12-OH-JA (and its derivatives 12-O-Glc-JA and 12-HSO4-JA) as a cleavage product of the JA-Ile catabolite 12OH-JA-Ile by the amido hydrolases IAR3 and ILL6. Our results identify the elusive 11OH-JA biosynthetic pathway and provide a revisited picture of JA metabolism where two separate enzyme systems lead to stress-modulated formation of hydroxy-JAs position isomers to attenuate signaling.

plant biology↗

bioRxiv2022

The S. cerevisiae m6A-reader Pho92 impacts meiotic recombination by controlling key methylated transcripts

N6-methyladenosine (m6A), the most abundant internal modification of eukaryotic mRNAs, participates in the post-transcriptional control of gene expression. In Saccharomyces cerevisiae, m6A is only found during meiosis. Although the deletion of the m6A- methyltransferase Ime4 impairs this process, the molecular impact of m6A on gene expression remains ill defined. Here we investigated the function of the budding yeast m6A reader Pho92. We found that Pho92 is specifically expressed during meiosis and impacts meiotic progression. We used high-throughput RNA sequencing and mapping of Pho92-binding sites following UV-crosslinking to show that Pho92 is recruited to specific mRNAs in an m6A-dependent manner during the meiotic prophase, preceding their down-regulation. Strikingly, point mutations altering m6A sites in mRNAs targeted by Pho92 are sufficient to delay their down-regulation and, in one case, to impact meiotic progression. Altogether, our results indicate that Pho92 facilitate the meiotic progression by accelerating the down-regulation of timely-regulated mRNAs during meiotic recombination.

molecular biology↗

bioRxiv2021

Nitrate-regulated growth processes involve activation of gibberellin pathway

Nitrate, one of the main nitrogen (N) sources for crops, acts as a nutrient and key signaling molecule coordinating gene expression, metabolism and various growth processes throughout the plant life cycle. It is widely accepted that nitrate-triggered developmental programs cooperate with hormone synthesis and transport, to finely adapt plant architecture to N availability. Here, we report that nitrate, acting through its signaling pathway, promotes growth in Arabidopsis and wheat, in part by modulating the accumulation of gibberellin (GA)-regulated DELLA growth repressors. We show that nitrate reduces the abundance of DELLAs by increasing GA contents through activation of GA metabolism gene expression. Consistently, the growth restraint conferred by nitrate deficiency is partially rescued in global-DELLA mutant that lacks all DELLAs. At the cellular level, we show that nitrate enhances both cell proliferation and elongation in a DELLA-dependent and -independent manner, respectively. Our findings establish a connection between nitrate and GA signaling pathways that allow plants to adapt their growth to nitrate availability.

plant biology↗

bioRxiv2020

Pioglitazone improves deficits of Fmr1-KO mouse model of Fragile X syndrome by interfering with excessive diacylglycerol signaling

Fragile X syndrome (FXS), the leading cause of familial intellectual disability, is an uncured disease caused by the absence or loss of function of the FMRP protein. FMRP is an RNA binding protein that controls the translation of specific proteins in neurons. A main target of FMRP in neurons is diacylglycerol kinase kappa (DGKk) and the loss of FMRP leads to a loss of DGK activity causing a diacylglycerol excess in the brain. Excessive diacylglycerol signaling could be a significant contributor to the pathomechanism of FXS. Here we tested the contribution of DAG-signaling in Fmr1-KO mouse model of FXS and we show that pioglitazone, a widely prescribed drug for type 2 diabetes, has ability to correct excessive DAG signaling in the brain and rescue behavioral alterations of the Fmr1-KO mouse. This study highlights the role of lipid signaling homeostasis in FXS and provides arguments to support the testing of pioglitazone for treatment of FXS.

neuroscience↗

bioRxiv2020

Function of the HYDROXYCINNAMOYL-CoA:SHIKIMATE HYDROXYCINNAMOYL TRANSFERASE is evolutionarily conserved in embryophytes

The plant phenylpropanoid pathway generates a major class of specialized metabolites and precursors of essential extracellular polymers that initially appeared upon plant terrestrialization. Despite its evolutionary significance, little is known about the complexity and function of this major metabolic pathway in extant bryophytes, which represent the non-vascular stage of embryophyte evolution. Here, we report that the HYDROXYCINNAMOYL-CoA:SHIKIMATE HYDROXYCINNAMOYL TRANSFERASE (HCT) gene that plays a critical function in the phenylpropanoid pathway during seed plant development, is functionally conserved in Physcomitrium patens (Physcomitrella), in the moss lineage of bryophytes. Phylogenetic analysis indicates that bonafide HCT function emerged in the progenitor of embryophytes. In vitro enzyme assays, moss phenolic pathway reconstitution in yeast and in planta gene inactivation coupled to targeted metabolic profiling, collectively indicate that P. patens HCT (PpHCT), similar to tracheophyte HCT orthologs, uses shikimate as a native acyl acceptor to produce a p-coumaroyl-5-O-shikimate intermediate. Phenotypic and metabolic analyses of loss-of-function mutants show that PpHCT is necessary for the production of caffeate derivatives, including previously reported caffeoyl-threonate esters, and for the formation of an intact cuticle. Deep conservation of HCT function in embryophytes is further suggested by the ability of HCT genes from P. patens and the liverwort Marchantia polymorpha to complement an Arabidopsis thaliana CRISPR/Cas9 hct mutant, and by the presence of phenolic esters of shikimate in representative species of the three bryophyte lineages.

plant biology↗

bioRxiv2019

Stress- and pathway-specific impacts of impaired jasmonoyl-isoleucine (JA-Ile) catabolism on defense signaling and biotic stress resistance in Arabidopsis

Jasmonate (JA) synthesis and signaling are essential for plant defense upregulation upon herbivore or microbial attacks. Stress-induced accumulation of jasmonoyl-isoleucine (JA-Ile), the bioactive hormonal form triggering major transcriptional changes, is often dynamic and transient, due to the existence of potent removal mechanisms. Two distinct but interconnected JA-Ile turnover pathways have been described in Arabidopsis, either via cytochrome P450 (CYP94)-mediated oxidation, or through deconjugation by the amidohydrolases (AH) IAR3 and ILL6. Their impact was not well known because of gene redundancy and compensation mechanisms when each pathway was partially impaired. Here we address the consequences of fully blocking either or both pathways on JA homeostasis and defense signaling in three mutant backgrounds: a double iar3 ill6 (2ah) mutant, a triple cyp94b1 b3 c1 mutant (3cyp), and a newly generated quintuple (5ko) mutant deficient in all known JA-Ile-degrading activities. These lines behaved very differently in response to either mechanical wounding, insect attack or fungal infection, highlighting the stress-specific contributions and impacts of JA-Ile catabolic pathways. Deconjugation and oxidative pathways contributed additively to JA-Ile removal upon wounding, but their genetic impairement had opposite impacts on Spodoptera littoralis larvae feeding: 2ah line was more resistant whereas 3cyp was more susceptible to insect attack. In contrast, 2ah, 5ko but not 3cyp overaccumulated JA-Ile upon inoculation by Botrytis cinerea, yet 3cyp was most resistant to the fungus. Despite of building-up unprecedented JA-Ile levels, 5ko displayed near WT levels of resistance in both bioassays. Molecular and metabolic analysis indicated that restrained JA-Ile catabolism resulted in enhanced defense and resistance levels only if genes encoding JAZ or JAM negative regulators were not simultaneously overstimulated. Our data demonstrate that despite of acting on a shared hormonal substrate, AH or/and CYP94 deficiency differentially impacts JA homeostasis, responses and tolerance to related biotic stresses.

plant biology↗

bioRxiv2019

RST1 and RIPR connect the cytosolic RNA exosome to the Ski complex in Arabidopsis

The RNA exosome is a key 3-5 exoribonuclease with an evolutionarily conserved structure and function. Its cytosolic functions require the co-factors SKI7 and the Ski complex. Here we demonstrate by co-purification experiments that the ARM repeat protein RESURRECTION1 (RST1) and RST1 INTERACTING PROTEIN (RIPR) connect the cytosolic Arabidopsis RNA exosome to the Ski complex. rst1 and ripr mutants accumulate RNA quality control siRNAs (rqc-siRNAs) produced by the post-transcriptional gene silencing (PTGS) machinery when mRNA degradation is compromised. The small RNA populations observed in rst1 and ripr mutants are also detected in mutants lacking the RRP45B/CER7 core exosome subunit. Thus, molecular and genetic evidence supports a physical and functional link between RST1, RIPR and the RNA exosome. Our data reveal the existence of additional cytosolic exosome co-factors besides the known SKI subunits. RST1 is not restricted to plants, as homologues with a similar domain architecture but unknown function exist in animals, including humans.

molecular biology↗