bioRxiv Science⌕ Search

Biology subjects

Peter, M.

Publications and source records attributed to Peter, M..

At least 19 recordsLinked to original sources

Monomeric TDP-43 binds GU-rich RNA via its NTD but only its oligomers block cryptic exon inclusion

TDP-43 aggregation is a pathological feature of several neurodegenerative diseases, resulting in nuclear loss of function and RNA dysregulation, including cryptic exon derepression. TDP-43 comprises two RNA recognition motifs required for canonical RNA binding, a low-complexity domain implicated in phase separation, and an N-terminal domain (NTD) that mediates oligomerization. While NTD-driven oligomerization is critical for TDP-43 splicing function, some studies suggest a direct interaction of NTD with RNA. Here, we investigated RNA binding by the NTD and its functional interplay with oligomerization. We show that the NTD preferentially binds UG-rich RNA via residues located at the oligomerization interface. The NTD engaged RNA only on monomeric TDP-43, as RNA binding and oligomerization compete for the same interface and rely on similar interaction modes. By disentangling these competing activities, we demonstrated that oligomerization, but not NTD-RNA interaction, is essential for TDP-43-dependent alternative splicing and repression of cryptic exons. Our findings uncover a previously unappreciated RNA-binding activity within the TDP-43 NTD that directly competes with oligomerization and establish oligomerization as a key determinant of TDP-43 cryptic exon repression.

molecular biology↗

Systematic identification of pH-sensing amyloid core motifs reveals a widespread mechanism for reversible protein assembly upon stress

Unlike irreversible pathological amyloids, reversible fibrils can be regulated via pH-sensing core motifs, characterized by amyloid properties unleashed upon stress-induced protonation of critical residues. Here, we combined bioinformatic predictions and an in vitro validation pipeline to search for pH-responsive, reversible amyloid core peptides in yeast and human proteomes. This approach uncovered biophysical properties distinguishing pH-sensing and constitutive amyloid cores and established reliable criteria to identify novel reversible assemblies based on sequence data. Selected full-length candidate proteins with evolutionarily conserved pH-sensing motifs were analyzed in Saccharomyces cerevisiae using fluorescence microscopy and SDS-resistance assays, revealing multiple proteins forming reversible assemblies in stationary phase. We found that protonation of a specific histidine in the amyloid core motif of the asparagine synthase Asn1 is necessary and sufficient for assembling catalytically inactive, reversible structures called cytoophidia. Interestingly, mutant cells that fail to assemble Asn1-cytoophidia show defects to recover from stationary phase, demonstrating functional relevance of pH-sensing amyloid core motifs in vivo. Taken together, we uncovered a widespread and conserved pH-sensing mechanism that regulates the reversible assembly and function of structurally diverse fibrils upon stress.

biochemistry↗

A preclinical resistance framework discovers the virulence risks of antibiotics in development

Several new antibiotics target multidrug-resistant pathogens, yet resistance is still evaluated mainly by drug-susceptibility, leaving consequences for bacterial pathogenicity poorly understood. Here, we develop a framework integrating resistance evolution, genomic surveillance and host-pathogen phenotyping to classify antibiotics by resistance potential and pathogenic consequences. Applying this framework to Klebsiella pneumoniae identified functionally distinct antibiotic candidates associated with elevated virulence risk. Resistance evolution rapidly increased virulence through clinically-relevant mutations, without direct selection for pathogenicity. Despite distinct genetic routes, resistance converged on cell-envelope rewiring. A single resistance mutation increased epithelial adhesion, intracellular colonization, macrophage immune-evasion, and tissue persistence in murine infection models, transforming K. pneumoniae into a more invasive and cytotoxic pathogen. Risk-profile analysis revealed partial decoupling of resistance and pathogenicity, with some low-resistance antibiotics yielding highly-virulent populations. These findings establish resistance-driven virulence as an underappreciated translational hazard and call for incorporating host-pathogen interactions into resistance surveillance and preclinical antibiotic development.

microbiology↗

Molecular determinants underlying substrate receptor specificity of human CRL4B E3 ubiquitin ligase

The vertebrate CRL4 family of Cullin-RING E3 ubiquitin ligases is distinguished from other cullin-based ligases by the presence of two highly homologous paralogs, CUL4A and CUL4B. Both CRL4 complexes use the DDB1 subunit to recruit dedicated and interchangeable substrate receptors called DCAFs, but the underlying mechanisms guiding DCAF specificity for CUL4B or CUL4A remain poorly understood. Here, we performed structural and biochemical analyses of the CRL4BLIS1 complex and identified two molecular determinants for CUL4B-specific DCAFs. First, we discovered that the unique CUL4B N-terminal extension directly binds CUL4B-specific DCAFs, enhancing their complex formation. This direct interaction can be modulated by phosphorylation, adding the possibility for spatiotemporal regulation. Second, the cryo-EM model of the CRL4BLIS1 complex identified a novel interface on the DDB1 subunit which promotes LIS1 recruitment. Quantitative affinity measurements and mutational analysis confirmed that this DDB1 interface is generally important for recruiting CUL4B-specific DCAFs including WDR1 and BRWD1, but not for CUL4A-specifc DCAFs, such as DCAF8. Together, our study identifies molecular determinants and unexpected interfaces on CRL4 components that dictate preference for DCAF recruitment. Graphical Abstract showing how the two CRL4 complexe s, namely CRL4A and CRL4B, recruit their DCAFs O_FIG O_LINKSMALLFIG WIDTH=186 HEIGHT=200 SRC="FIGDIR/small/711546v1_ufig1.gif" ALT="Figure 1000"> View larger version (39K): org.highwire.dtl.DTLVardef@10e476eorg.highwire.dtl.DTLVardef@73a405org.highwire.dtl.DTLVardef@1571a1org.highwire.dtl.DTLVardef@1d70946_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

Compressive mechanical stress activates ERK5 to regulate cortical tension and promote invasive cellular traits

Growth-induced compressive forces regulate diverse biological processes ranging from development to tumor progression, but the underlying molecular mechanisms remain poorly understood. Here, we found that compressive mechanical cues activate the MAP kinase extracellular signal-regulated kinase 5 (ERK5) at the cell periphery, inducing invasive traits in epithelial cells. Using a phospho-proteomic approach combined with an RNAi-based validation screen, we identified several previously unrecognized ERK5 effectors important for cell-cell adhesion and actin organization, among them the myosin light chain (MLC) phosphatase subunit Myosin Phosphatase-Targeting Subunit 1 (MYPT1). Our results demonstrate that ERK5 regulates MYPT1, which in turn inhibits myosin at the cell periphery. ERK5 signaling counteracts Rho-associated protein kinase (ROCK), thereby reducing peripheral actomyosin tension. This relaxation destabilizes cell-cell contacts and promotes cell migration in response to mechanical compression. Together, these findings identify an ERK5-mediated response mechanism activated by compressive force that triggers cell invasion, highlighting ERK5 therapeutic potential.

cell biology↗

Lysosomal escape and TMEM106B fibrillar core determine TDP-43 seeding outcomes

Frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) shows striking clinical and neuropathological heterogeneity, yet a systematic analysis of subtype-specific features and inter-patient variability was missing. We treated human neurons and neuron-like cells with 30 postmortem brain samples and quantified neoaggregate formation, loss of function and changes in the TDP-43 interactome to define determinants of seeding outcomes. Potent FTLD-TDP-A seeds drove a progressive collapse of physiological TDP-43 interactions accompanied by functional loss. Beyond the burden of pathological TDP-43, we identified the fibrillar core of the lysosomal protein TMEM106B as a critical pro-seeding factor. Transient lysosomal injury markedly enhanced neoaggregation and loss of function, likely by promoting fibril interactions with native TDP-43. Our work establishes a mechanistic link between TMEM106B and TDP-43 aggregation, identifies lysosomal escape as a key driver of pathology and introduces the strongest model yet for seeded TDP-43 aggregation and loss of function, to enable discovery of disease modifiers.

neuroscience↗

Adaptation of eukaryotic membrane homeostasis to species-specific cellular lipid landscapes

The physicochemical properties of biological membranes must be maintained within a range compatible with cellular physiology. In the face of external perturbations, membrane lipid homeostasis mechanisms sense and control membrane features. How such mechanisms evolve to function in organisms with different cellular lipid make-up is unknown. Here, we address this fundamental question by exploiting the natural divergence in membrane lipid composition between the related fission yeasts S. pombe and S. japonicus. Using lipidomics and transcriptomics, we show that the activity of the membrane-bound transcriptional activator Mga2, which regulates the {Delta}-9 desaturase Ole1 expression, is set to sense distinct levels of membrane unsaturation in the two species. Through retro-engineering and physiological experiments, we identify an evolutionary divergent but functionally constrained element within the juxtamembrane region of Mga2, which fine-tunes its performance to species-specific lipid composition. Our experiments indicate that high baseline expression of ole1, set by cis-regulatory elements in its upstream non-coding region, has redefined the dynamic range of Mga2 activation in S. pombe, supporting high lipidome unsaturation. Our work explores an "experiment of nature" to highlight the broad principles underlying the organisation and evolution of membrane homeostasis, which should be applicable to other genetic networks supporting cellular homeostatic processes.

cell biology↗

Limited Effects of Isolated Congenital Anosmia on Cerebral White Matter Morphology

Lack of sensory input is associated with alterations in brain morphology; mainly in or near cerebral regions normally devoted to processing of the missing sense. We have in multiple studies demonstrated that the only consistent morphological finding within the gray matter of individuals born without the sense of smell (isolated congenital anosmia; ICA), are changes in or near the olfactory sulcus. For the connecting tissue of the brain, the white matter (WM), previous studies have yielded inconsistent findings. Here, we show that individuals with ICA (n=49) exhibit alterations in WM volume as compared to age- and sex-matched controls. Consistent evidence from both voxel-based morphometry and multi-voxel pattern analysis shows that individuals with ICA show decreased WM in areas surrounding the olfactory sulcus. Importantly, no WM alterations were found in areas surrounding the olfactory (piriform) cortex. In contrast to congenital sensory loss in other systems, we show that morphological alterations due to lifelong olfactory deprivation are limited. Alterations are primarily localized around the olfactory sulcus and likely due to the absence of olfactory bulbs. A possible explanation for the lack of major morphological alterations in individuals with congenital anosmia is that the olfactory regions may be recruited for non-olfactory functions.

neuroscience↗

Disruption of nucleolar integrity triggers cellular quiescence through organelle rewiring and secretion

The nucleolus is the largest membraneless nuclear organelle and a critical regulator of growth and stress responses, comprised of over 600 proteins involved in ribosome biogenesis. However, how the nucleolar function and architecture coordinate cell-wide adaptive programs remains unclear. Here, we combined multi-omics profiling with functional genomics to define the cellular consequences of nucleolar disruption. We identify a stress response pathway connecting the nucleolus to the Golgi apparatus, endo-lysosomal trafficking, and cellular secretion (NuGETS). Chronic nucleolar defects activate a TP53-dependent transcriptional program that promotes organelle expansion, enhances secretory activity, and induces cell cycle exit with prolonged quiescence and partial epithelial-to-mesenchymal transition (pEMT) phenotypes. A genome-wide CRISPRi screen uncovered 400 regulators of secretory and quiescent states upon nucleolar stress. These pathways are enriched in cancer progression associated with ribosomopathies. Our findings therefore link nucleolar stress responses and cancer development, revealing cell-wide regulatory mechanisms that safeguard survival when nucleolar function is compromised.

cell biology↗

PKA regulates stress granule maturation to allow timely recovery after prolonged starvation

Cells have evolved multiple strategies to survive environmental stress conditions. This includes the formation of membrane-less cytoplasmic ribonucleoprotein structures called stress granules (SGs) that sequester and protect mRNAs encoding many housekeeping genes. SGs are not static biomolecular condensates but transform into solid states during a maturation phase. Although SG maturation is a hallmark of many neurodegenerative pathologies, little is known about the mechanisms and physiological relevance underlying the maturation process. Here we show that yeast SGs mature into a solid-like state during long-term stationary phase stress, which delays SG disassembly and cell cycle restart. Profiling of phosphorylation sites during stationary phase revealed that SG maturation is driven by protein kinase A (PKA)-dependent phosphorylation of the SG proteome. Indeed, upon stationary phase the catalytic PKA subunits condense in SGs where they maintain kinase activity, while during this time cytoplasmic PKA is inhibited. PKA-mediated phosphorylation of key SG components, like the pyruvate kinase Cdc19, is necessary and sufficient for its timely accumulation in SGs, where Cdc19 assembles into amyloid-like structures. Importantly, inhibiting PKA during long-term stationary phase prevents SG maturation, delaying ordered re-start of cell growth after re-feeding. Taken together, these results describe a SG maturation mechanism, selectively activated during chronic stress, that preserves SG integrity and promotes cell survival. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=164 HEIGHT=200 SRC="FIGDIR/small/663161v1_ufig1.gif" ALT="Figure 1"> View larger version (25K): org.highwire.dtl.DTLVardef@19c4d82org.highwire.dtl.DTLVardef@a4cf27org.highwire.dtl.DTLVardef@1c2577org.highwire.dtl.DTLVardef@1dfe84f_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIStress granules mature during chronic stress such as long-term stationary phase C_LIO_LIPhosphorylation of SG components by PKA is a hallmark of SG maturation C_LIO_LIPhosphorylation of Cdc19 by PKA promotes its maturation into an amyloid-like state C_LIO_LISG maturation acts as a timer for recovery after chronic stress C_LI

cell biology↗

Prevalence of water and nutrient availability in structuring fungal communities of healthy and decaying beech trees in forests

Background and aimsIn forest ecosystems, trees interact with a broad range of soil microorganisms, such as ectomycorrhizal fungi, improving nutrition and water uptake and mitigating biotic and abiotic stress. In the context of the predicted more frequent and more severe droughts, it is critical to characterise how trees and their associated fungal partners respond to water shortage to improve future forest management. MethodsWe investigated the importance of diverse environmental predictors (e.g., edaphic, climatic, topographic) on the fungal communities associated with the root systems of decaying and healthy beech trees in natural beech forests. In parallel, we identified specific fungal taxa linked with their host vitality and water stress gradient. ResultsWe observed that soil water shortage had a greater effect on the structuring of fungal communities than beech vitality or other environmental factors. We identified a core group of fungi that remained unaffected by water availability among all study sites, while other fungal species were more abundant in sampling sites more prone to water shortage. Finally, we showed that the abundance of ectomycorrhizal fungi was significantly associated with healthy beech root systems, while saprotrophic fungi prevailed in the roots of trees exhibiting severe decay. ConclusionsOverall, our study highlights the major role of drought in structuring fungal communities associated with beech root systems and pinpoints the key fungal taxonomic groups found in healthy beech trees.

ecology↗

EGFR activation in cholangiocytes promotes extrahepatic bile duct regeneration after injury

Background & AimsThe epidermal growth factor (EGF) receptor family of tyrosine kinases regulates development and homeostasis of digestive organs including the liver and bile ducts. It consists of four receptors, EGF receptor (EGFR) and erythroblastoma oncogene B 2-4 (ERBB2-4), and their corresponding ligands. EGF signaling promotes intrahepatic cholangiocyte proliferation, bipotent cell transdifferentiation into cholangiocytes, bile duct branching, and cholangiocarcinoma (CCA) aggressiveness. The EGF family signaling contribution to extrahepatic bile duct (EHBD) regeneration is not well defined. This work is aimed at determining the fundamental role of the EGF signaling network in the biliary proliferative response to EHBD obstruction. ApproachWe used mouse bile duct ligation to model obstructive EHBD injury, and human and mouse EHBD organoids for in vitro studies. We tested activating and inhibitory paradigms with recombinant EGF family ligands and receptor antagonists. Transcriptomic and immunohistochemistry analyses informed EGF signaling changes and cellular localization at homeostasis and after obstruction. ResultsAt homeostasis, the EHBD expressed EGFR ligands Tgfa, Btc, Hb-egf and Nrg4 in cholangiocytes, and Egf in stromal cells. Erbb2 and Erbb3 were predominant receptors expressed in cholangiocytes and Egfr in stromal cells at baseline. After EHBD obstruction, injury-induced biliary hyperproliferation was associated with increased abundance of Areg, Hb-egf, Tgf and Btc ligands and Egfr receptor in cholangiocytes with resulting epithelial EGFR activation. In biliary organoids, EGFR ligands induced organoid growth, and inhibition of EGFR, but not ERBB2, dampened cholangiocyte proliferation. Accordingly, EGFR inhibition in mice led to a decrease in the biliary proliferative response after EHBD obstruction. ConclusionThe obstruction-induced biliary proliferation is an EGFR-mediated response suggesting context-and receptor-specific EGF signaling network involvement in EHBD regeneration after injury.

physiology↗

Comparative transcriptomics uncovers plant and fungal genetic determinants of mycorrhizal compatibility

Ectomycorrhizal symbiosis supports tree growth and is crucial for nutrient cycling and temperate and boreal ecosystems functioning. The establishment of functional ECM first requires the association of compatible partners. However, host and fungal genetic determinants governing mycorrhizal compatibility are unknown. To identify such factors in poplar and its fungal associates, we mined existing and de-novo tree and fungal transcriptional datasets. We identified core plant regulons enabling ECM symbiosis at early and mature stages of the interaction. These regulons can be divided into general fungal-sensing and ECM-specific components. We highlight the importance of fungal modulation of plant JA-related defences and the regulation of secretory pathways for ECM compatibility, including upregulation of key fungal small secreted proteins, the downregulation of plant secreted peroxidases and the downregulation of plant cell-wall remodelling proteins concomitantly with the upregulation of fungal glycosyl hydrolases acting on pectin. Not only gene-regulation, but also its temporal scale and dynamics seems to play a crucial role for mycorrhizal compatibility. The expression profile of the host Common Symbiosis Pathway was also studied, revealing constitutive levels of expression of a part of the pathway and moderate upregulation in compatible ECM interactions. Overall, these results underscore the importance of novel biological functions during the establishment of ECM symbiosis, help us gain insights into the molecular events determining mycorrhiza compatibility and serve as a data-rich transcriptomic resource to open new research questions in the field. Significance statementEctomycorrhizal symbiosis is essential for forest ecosystems, but the genetic determinants of host and fungal compatibility remain underexplored. Employing comparative transcriptomics, we identified plant general and ECM-specific gene regulons, outlining the expression profile of Common Symbiosis Pathway genes in multiple ECM interactions and highlighting fungal and plant genes associated to interkingdom crosstalk and cell wall remodelling. These findings help us gain insights into the molecular events determining mycorrhiza compatibility.

plant biology↗

Fatty acid synthesis supports tumor progression through keeping TORC1 receptive for Insulin/PI3K signaling

Biosynthesis of lipids and fatty acids (FAs) is a tightly regulated and complex process essential for the normal functioning of various cellular processes as is sufficient lipid availability for the progression of several malignant tumor types. Despite its importance, the roles of the individual steps in lipid biosynthesis during tumor growth and their subsequent interaction with intracellular signaling pathways are still not well understood. In our study, we used the RasV12, Scribble deficient carcinoma model in Drosophila to demonstrate that upregulation of de novo FA and lipid synthesis is a conserved characteristic of malignant tumors. Performing a small-scale genetic screen by tumor cell specific silencing of components of neutral lipid biosynthetic apparatus revealed that the loss of several enzymes involved in FA and diacylglycerol synthesis significantly inhibited tumor growth. Further characterization of the role of acetyl-CoA carboxylase (ACC), the enzyme responsible for the first step of FA synthesis, revealed that loss of ACC significantly reduced late-stage tumor growth due to increased apoptotic activity. However, early tumor development was unaffected. This correlated with our observation that perturbation of FA synthesis led to inactivation of TORC1 (Target of Rapamycin Complex 1) - the master regulator of cell growth and survival - accompanied by activation of the catabolic process autophagy. Moreover, we also demonstrated that TORC1 activity cannot be restored by hyperactivation of upstream Insulin/PI3K signaling or inhibition of AMP-activated kinase (AMPK) in ACC deficient tumor cells but supplementation of ACC deficient tumors with ectopically added oleic acid alone could improve TORC1 activity and thereby tumor progression. Hence, our findings highlight a new role of FAs in regulating TORC1, rendering it receptive to upstream activatory signals, explaining why cancer cells are extremely dependent on de novo FA synthesis.

cell biology↗

Altered neuronal network activity and connectivity in human Down Syndrome excitatory cortical neurons

Down syndrome (DS) is the most common genetic cause of intellectual disability, affecting one in 700 live births worldwide, and is caused by trisomy of the human chromosome 21 (Hsa21), yet the cellular and molecular mechanisms driving neuronal network dysfunction remain poorly understood. Here, we investigated whether trisomy 21 (TS21) alters the spontaneous synchronised activity of excitatory neuron networks, potentially contributing to the neurodevelopmental phenotypes of DS. By modelling human cortical development in vitro with TS21 and matched control human iPSCs from two DS donors, we investigated the impact of Hsa21 triplication on neural network activity and connectivity. Calcium imaging revealed an early and pronounced reduction in neuronal activity in TS21 cortical neurons, including a marked loss of synchronised bursting. These deficits persisted up to 80 days in vitro and for over 5 months in vivo following transplantation into the mouse forebrain, as shown by multiphoton calcium imaging through a cranial window. Viral trans-synaptic tracing identified significant reduction of neuronal connectivity in TS21 neuronal networks in vitro, suggesting that reduced network connectivity contributes to the dramatic reduction of synchronised bursting. Furthermore, TS21 neurons displayed significantly reduced expression of voltage-gated potassium channels, with single-neuron recordings confirming a reduction of hyperpolarization-activated currents. Together, these findings demonstrate long-lasting impairments in human cortical excitatory neuron network function associated with Trisomy 21.

neuroscience↗

Horizontal gene transfer-initiated reorganization of lipid metabolism drives lifestyle innovation in a eukaryote

Horizontal gene transfer is a source of metabolic innovation and adaptation to new environments. Yet, how horizontally transferred metabolic functionalities are integrated into host cell biology remains an open question. Here, we use the fission yeast Schizosaccharomyces japonicus to probe how eukaryotic lipid metabolism is rewired in response to the acquisition of a horizontally transferred squalene-hopene cyclase Shc1. We show that Shc1-dependent production of hopanoids, the structural mimics of eukaryotic sterols, allows S. japonicus to thrive in anoxia, where sterol biosynthesis is not possible. We further demonstrate that glycerophospholipid fatty acyl asymmetry, prevalent in S. japonicus, is crucial for accommodating both sterols and hopanoids in membranes, and explain how Shc1 functions alongside the native sterol biosynthetic pathway to support membrane properties. Through engineering experiments in the sister species S. pombe, which naturally lacks Shc1, we show that the acquisition of Shc1 may entail new physiological traits; however, to maximize Shc1 performance, sterol biosynthesis must be dampened. Our work sheds new light on the mechanisms underlying cellular integration of horizontally transferred genes in eukaryotes and provides broader insights into the evolution of membrane organization and function.

cell biology↗

Mild hyperthermia-induced thermogenesis in the endoplasmic reticulum defines stress response mechanisms

Previous studies reported that a mild, non-protein denaturing, fever-like temperature increase induced the unfolded protein response (UPR) in mammalian cells. Our dSTORM super-resolution microscopy experiments revealed that the master regulator of the UPR, the IRE1 (inositol-requiring enzyme 1) protein is clustered as a result of UPR activation in a human osteosarcoma cell line (U2OS) upon mild heat stress. Using ER thermo yellow, a temperature-sensitive fluorescent probe targeted to the endoplasmic reticulum (ER), we detected significant intracellular thermogenesis in mouse embryonic fibroblast (MEF) cells. Temperatures reached at least 8{degrees}C higher than the external environment (40{degrees}C), resulting in exceptionally high ER temperatures similar to those previously described for mitochondria. Mild heat-induced thermogenesis in the ER of MEF cells was likely due to the uncoupling of the Ca2+/ATPase (SERCA) pump. The high ER temperatures initiated a pronounced cytosolic heat shock response in MEF cells, which was significantly lower in U2OS cells in which both the ER thermogenesis and SERCA pump uncoupling were absent. Our results suggest that, depending on intrinsic cellular properties, mild hyperthemia-induced intracellular thermogenesis defines the cellular response mechanism, and determines the outcome of hyperthermic stress.

cell biology↗

Stm1 regulates Ifh1 activity revealing crosstalk between ribosome biogenesis and ribosome dormancy

Ribosome abundance in changing environments is governed by biogenesis and degradation, but the underlying mechanisms regulating these opposing processes remain unknown. Here we show that Suppressor of Tom1 (Stm1), a dormancy factor protecting cytosolic ribosomes during starvation, has an unexpected function to promote ribosome biogenesis during exponential growth conditions. Indeed, Stm1 transiently localizes to the nucleolus and engages with pre-ribosomal particles. Stm1 upregulates transcription of ribosomal protein genes by directly binding the activation domain (AD) of the transcription factor Ifh1. These novel Stm1 functions confer rapamycin-sensitivity and are mediated by its C-terminal intrinsically disordered region (IDR), which is dispensable for ribosome hibernation. We conclude that Stm1 regulates ribosome homeostasis linking ribosome biogenesis and ribosome dormancy.

cell biology↗