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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 19 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2024

Post-translational modifications: emerging directors of cell-fate decisions during endoplasmic reticulum stress in Arabidopsis thaliana

Homeostasis of the endoplasmic reticulum (ER) is critical for growth, development, and stress responses. Perturbations causing an imbalance in ER proteostasis lead to a potentially lethal condition known as ER stress. In ER stress situations, cell-fate decisions either activate pro-life pathways that reestablish homeostasis or initiate pro-death pathways to prevent further damage to the organism. Understanding the mechanisms underpinning cell-fate decisions in ER stress is critical for crop development and has the potential to enable translation of conserved components to ER stress-related diseases in metazoans. Post-translational modifications (PTMs) of proteins are emerging as key players in cell-fate decisions in situations of imbalanced ER proteostasis. In this review, we address PTMs orchestrating cell-fate decisions in ER stress in plants and provide evidence-based perspectives for where future studies may focus to identify additional PTMs involved in ER stress management.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2023

An IRE1-proteasome system signalling cohort controls cell fate determination in unresolved proteotoxic stress of the plant endoplasmic reticulum

Excessive accumulation of misfolded proteins in the endoplasmic reticulum (ER) causes ER stress, which is an underlying cause of major crop losses and devastating human conditions. Here, ER proteostasis surveillance is mediated by the conserved master regulator of the unfolded protein response (UPR), Inositol Requiring Enzyme 1 (IRE1), which determines cell fate by controlling pro-life and pro-death outcomes through as yet largely unknown mechanisms. Here we report that Arabidopsis IRE1 determines cell fate in ER stress by balancing the ubiquitin–proteasome system (UPS) and UPR through the plant-unique E3 ligase, PHOSPHATASE TYPE 2CA (PP2CA)-INTERACTING RING FINGER PROTEIN 1 (PIR1). Indeed, PIR1 loss leads to suppression of pro-death UPS and the lethal phenotype of an IRE1 loss-of-function mutant in unresolved ER stress in addition to activating pro-survival UPR. Specifically, in ER stress, PIR1 loss stabilizes ABI5, a basic leucine zipper (bZIP) transcription factor, that directly activates expression of the critical UPR regulator gene, bZIP60, triggering transcriptional cascades enhancing pro-survival UPR. Collectively, our results identify new cell fate effectors in plant ER stress by showing that IRE1’s coordination of cell death and survival hinges on PIR1, a key pro-death component of the UPS, which controls ABI5, a pro-survival transcriptional activator of bZIP60.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2025

PCM1 coordinates centrosome asymmetry with polarized endosome dynamics to regulate daughter cell fate

Vertebrate radial glia progenitors (RGPs) balance self-renewal and differentiation through asymmetric cell division (ACD), which involves unequal centrosome inheritance. How centrosome asymmetry directs cell fate remains poorly understood. Here, we identify Pericentriolar material 1 (Pcm1) as a key player in this process. In zebrafish embryonic RGPs, Pcm1 is asymmetrically associated with Cep83, a mother centrosome marker. Using in vivo time-lapse imaging and nanoscale-resolution expansion microscopy, we detect Pcm1 on Notch ligand-containing endosomes, where it interacts–either directly or indirectly–with Par-3 and dynein. Loss of pcm1 disrupts endosome dynamics, increasing neuronal differentiation at the expense of RGP self-renewal. Mechanistically, Pcm1 facilitates the transition from Rab5b to Rab11a and promotes the assembly of Par-3 and dynein macromolecular complexes on recycling endosomes. Furthermore, we find conserved PARD3-PCM1-CEP83-RAB11 associations in human cortical brain organoids. Our findings uncover that Pcm1 links centrosome asymmetry to polarized endosome trafficking, thereby regulating RGP fate decisions.

Cell fate and cell lineage↗
DOE OSTI2024

Chloroplast Stress Signals: Control of Retrograde Signaling, Chloroplast Turn-Over, and Cell Fate Decisions

Chloroplasts (photosynthetic plastids) are semiautonomous organelles that contain their own small genomes. The proteomes of chloroplasts, however, are a mixture of plastid and nuclear-encoded proteins. Chloroplasts perform photosynthesis, which is prone to damaging the organelles, leading to the production of reactive oxygen species (ROS) that damage the cell under environmental stresses. Thus, for the cell to maintain proper chloroplast function, efficient photosynthesis, and avoid ROS damage, it relies on complex crosstalk between the chloroplast, the nucleus, other organelles within the cell, and the cytoplasm in between. This communication involves retrograde signals from chloroplasts to control nuclear gene expression, programmed cell death (PCD), and chloroplast degradation. Here we review these signals with an emphasis on the roles of the ROS singlet oxygen ( 1 O 2 ) and plastid gene expression. We cover (1) recent work on understanding how multiple 1 O 2 signaling pathways can be initiated within stressed chloroplasts, (2) how individualized post-translational regulatory systems allow chloroplasts to control their proteomes and degradation, and (3) how chloroplast signals ultimately control cell fate decisions, such as PCD, senescence, and vacuole-mediated degradation of chloroplasts (chloroplast quality control). Overall, this chapter discusses how chloroplasts can act as environmental sensors for the cell and allow plants to acclimate to stress and thrive in dynamic environments.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2023

Gibberellins promote polar auxin transport to regulate stem cell fate decisions in cambium

Vascular cambium contains bifacial stem cells, which produce secondary xylem to one side and secondary phloem to the other. However, how these fate decisions are regulated is unknown. Here we show that the positioning of an auxin signalling maximum within the cambium determines the fate of stem cell daughters. The position is modulated by gibberellin-regulated, PIN1-dependent polar auxin transport. Gibberellin treatment broadens auxin maximum from the xylem side of the cambium towards the phloem. As a result, xylem-side stem cell daughter preferentially differentiates into xylem, while phloem-side daughter retains stem cell identity. Occasionally, this broadening leads to direct specification of both daughters as xylem, and consequently, adjacent phloem-identity cell reverts to being stem cell. Conversely, reduced gibberellin levels favour specification of phloem-side stem cell daughter as phloem. Together, our data provide a mechanism by which gibberellin regulates the ratio of xylem and phloem production.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2024

Water acidification aggravates lithium-induced toxicity represented by energy supply, oxidative stress, and cell fate in Daphnia magna neonates

Lithium is extensively utilized in industrial energy production, particularly in lithium-ion batteries, and in pharmaceuticals for the treating clinical mood disorders. Consequently, lithium is frequently detected in various environmental matrices. It has been reported to cause a range of toxic effects on aquatic organisms including oxidative stress, neurological disorders, and reproductive suppression. Water acidification is a global issue with numerous negative impacts on aquatic organisms. It can alter the physio-chemical properties and bioavailability of metal ions. The acidic leaching process during lithium battery treatment and global water acidification both suggest that lithium contamination often occurs in acidic environments. In the present study, Daphnia magna neonates were exposed to four treatments (control, lithium alone, low pH, and combined) to investigate whether an acidic environment exacerbates the toxic effects of lithium on aquatic organisms and to explore potential toxic action mechanisms. The results indicated that low pH posed a significant threat to the growth and reproduction of D. magna. When exposed to both lithium and low pH, there was increased lithium accumulation and an energy trade-off response, leading to increased energy allocation to reproduction and reduced energy for growth. Lithium exposure stimulated D. magna activity, while low pH inhibited it, suggesting that an imbalance in energy consumption and supply. Combined exposure to lithium and low pH resulted in severe oxidative stress due to mitochondrial dysfunction, under-utilization of energy substances, and increased ionic homeostasis disturbances. Consequently, the exposed organism altered apoptosis and autophagy processes to maintain homeostasis. In conclusion, the present study demonstrated that lithium and water acidification posed a population-level threat to D. magna, and their combined exposure significantly largely exacerbated the toxic effects.

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTAN↗
DOE OSTI2022

Regulators of early maize leaf development inferred from transcriptomes of laser capture microdissection (LCM)-isolated embryonic leaf cells

The superior photosynthetic efficiency of C 4 leaves over C 3 leaves is owing to their unique Kranz anatomy, in which the vein is surrounded by one layer of bundle sheath (BS) cells and one layer of mesophyll (M) cells. Kranz anatomy development starts from three contiguous ground meristem (GM) cells, but its regulators and underlying molecular mechanism are largely unknown. To identify the regulators, we obtained the transcriptomes of 11 maize embryonic leaf cell types from five stages of pre-Kranz cells starting from median GM cells and six stages of pre-M cells starting from undifferentiated cells. Principal component and clustering analyses of transcriptomic data revealed rapid pre-Kranz cell differentiation in the first two stages but slow differentiation in the last three stages, suggesting early Kranz cell fate determination. In contrast, pre-M cells exhibit a more prolonged transcriptional differentiation process. Differential gene expression and coexpression analyses identified gene coexpression modules, one of which included 3 auxin transporter and 18 transcription factor (TF) genes, including known regulators of Kranz anatomy and/or vascular development. In situ hybridization of 11 TF genes validated their expression in early Kranz development. We determined the binding motifs of 15 TFs, predicted TF target gene relationships among the 18 TF and 3 auxin transporter genes, and validated 67 predictions by electrophoresis mobility shift assay. From these data, we constructed a gene regulatory network for Kranz development. Our study sheds light on the regulation of early maize leaf development and provides candidate leaf development regulators for future study.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2023

Model certainty in cellular network-driven processes with missing data

Mathematical models are often used to explore network-driven cellular processes from a systems perspective. However, a dearth of quantitative data suitable for model calibration leads to models with parameter unidentifiability and questionable predictive power. Here we introduce a combined Bayesian and Machine Learning Measurement Model approach to explore how quantitative and non-quantitative data constrain models of apoptosis execution within a missing data context. We find model prediction accuracy and certainty strongly depend on rigorous data-driven formulations of the measurement, and the size and make-up of the datasets. For instance, two orders of magnitude more ordinal (e.g., immunoblot) data are necessary to achieve accuracy comparable to quantitative (e.g., fluorescence) data for calibration of an apoptosis execution model. Notably, ordinal and nominal (e.g., cell fate observations) non-quantitative data synergize to reduce model uncertainty and improve accuracy. Finally, we demonstrate the potential of a data-driven Measurement Model approach to identify model features that could lead to informative experimental measurements and improve model predictive power.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2024

Combinatorial transcription factor binding encodes cis -regulatory wiring of mouse forebrain GABAergic neurogenesis

Transcription factors (TFs) bind combinatorially to cis-regulatory elements, orchestrating transcriptional programs. Although studies of chromatin state and chromosomal interactions have demonstrated dynamic neurodevelopmental cis-regulatory landscapes, parallel understanding of TF interactions lags. To elucidate combinatorial TF binding driving mouse basal ganglia development, we integrated chromatin immunoprecipitation sequencing (ChIP-seq) for twelve TFs, H3K4me3-associated enhancer-promoter interactions, chromatin and gene expression data, and functional enhancer assays. We identified sets of putative regulatory elements with shared TF binding (TF-pRE modules) that orchestrate distinct processes of GABAergic neurogenesis and suppress other cell fates. The majority of pREs were bound by one or two TFs; however, a small proportion were extensively bound. These sequences had exceptional evolutionary conservation and motif density, complex chromosomal interactions, and activity as in vivo enhancers. Our results provide insights into the combinatorial TF-pRE interactions that activate and repress expression programs during telencephalon neurogenesis and demonstrate the value of TF binding toward modeling developmental transcriptional wiring.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2024

Programmed cell death regulator BAP2 is required for IRE1-mediated unfolded protein response in Arabidopsis

Environmental and physiological situations can challenge the balance between protein synthesis and folding capacity of the endoplasmic reticulum (ER) and cause ER stress, a potentially lethal condition. The unfolded protein response (UPR) restores ER homeostasis or actuates programmed cell death (PCD) when ER stress is unresolved. The cell fate determination mechanisms of the UPR are not well understood, especially in plants. Here, we integrate genetics and ER stress profiling with natural variation and quantitative trait locus analysis of 350 natural accessions of the model species Arabidopsis thaliana . Our analyses implicate a single nucleotide polymorphism to the loss of function of the general PCD regulator BON-ASSOCIATED PROTEIN2 (BAP2) in UPR outcomes. We establish that ER stress-induced BAP2 expression is antagonistically regulated by the UPR master regulator, inositol-requiring enzyme 1 (IRE1), and that BAP2 controls adaptive UPR amplitude in ER stress and ignites pro-death mechanisms in conditions of UPR insufficiency.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2025

SOX2-driven enhancer landscape defines the transcriptional architecture of retinogenesis

Retinal neurogenesis is mediated by the coordinated activities of a complex gene regulatory network (GRN) of transcription factors (TFs) in multipotent retinal progenitor cells (RPCs). How this GRN mechanistically guides neural competence remains poorly understood. In this study, we present integrated transcriptional, genetic and genomic analyses to uncover the regulatory mechanisms of SOX2, a key factor in establishing neural identity in RPCs. We show that SOX2 is preferentially enriched in the RPC-specific enhancer landscape associated with essential regulators of retinogenesis. Disruption of SOX2 expression impairs retinogenesis, marked by a selective loss of enhancer activity near genes essential for RPC proliferation and lineage specification. We identified the RPC transcription factor VSX2 as a binding partner for SOX2 and, together, SOX2 and VSX2 co-target a core, retina-specific chromatin repertoire characterized by enhanced TF binding and robust chromatin accessibility. This cooperative binding establishes a shared SOX2-VSX2 transcriptional code that promotes the expression of crucial regulators of neurogenesis while repressing the acquisition of alternative lineage cell fate. Our data illuminate fundamental biological insights on how transcription factors act in concert to drive chromatin-based genetic programs underlying retinal neural identity.

Chromatin↗
DOE OSTI2022

Why are cell populations maintained via multiple compartments?

We consider the maintenance of ‘product’ cell populations from ‘progenitor’ cells via a sequence of one or more cell types, or compartments, where each cell’s fate is chosen stochastically. If there is only one compartment then large amplification, that is, a large ratio of product cells to progenitors comes with disadvantages. The product cell population is dominated by large families (cells descended from the same progenitor) and many generations separate, on average, product cells from progenitors. These disadvantages are avoided using suitably constructed sequences of compartments: the amplification factor of a sequence is the product of the amplification factors of each compartment, while the average number of generations is a sum over contributions from each compartment. Passing through multiple compartments is, in fact, an efficient way to maintain a product cell population from a small flux of progenitors, avoiding excessive clonality and minimizing the number of rounds of division en route. We use division, exit and death rates, estimated from measurements of single-positive thymocytes, to choose illustrative parameter values in the single-compartment case. We also consider a five-compartment model of thymocyte differentiation, from double-negative precursors to single-positive product cells.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2025

Sorted-cell proteomics reveals an AT1-associated epithelial cornification phenotype and suggests endothelial redox imbalance in human bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) is a neonatal lung disease characterized by inflammation and scarring leading to long-term tissue damage. Previous whole tissue proteomics identified BPD-specific proteome changes and cell type shifts. Little is known about the proteome-level changes within specific cell populations in disease. Here, we sorted epithelial (EPI) and endothelial (ENDO) cell populations based on their differential surface markers from normal and BPD human lungs. Using a low-input compatible sample preparation method (MicroPOT), proteins were extracted and digested into peptides and subjected to liquid chromatography-tandem mass spectrometry (LC-MS/MS) proteome analysis. Of the 4,970 proteins detected, 293 were modulated in abundance or detection in the EPI population and 422 were modulated in ENDO cells. Modulation of proteins associated with actin-cytoskeletal function, such as SCEL, LMO7, and TBA1B was observed in the BPD EPIs. Using confocal imaging and analysis, we validated the presence of aberrant multilayer-like structures comprising SCEL and LMO7, known to be associated with epidermal cornification, in the human BPD lung. This is the first report of the accumulation of cornification-associated proteins in BPD. Their localization in the alveolar parenchyma, primarily associated with alveolar type 1 (AT1) cells, suggests a role in the BPD postinjury response. In the ENDOs, redox balance and mitochondrial function pathways were modulated. Alternative mRNA splicing and cell proliferative functions were elevated in both populations, suggesting potential dysregulation of cell progenitor fate. This study characterized the proteome of epithelial and endothelial cells from the BPD lung for the first time, identifying population-specific changes in BPD pathogenesis.

BPD↗
DOE OSTI2024

Biophysical and Structural Features of αβT ‐Cell Receptor Mechanosensing: A Paradigmatic Shift in Understanding T‐Cell Activation

ABSTRACT αβT cells protect vertebrates against many diseases, optimizing surveillance using mechanical force to distinguish between pathophysiologic cellular alterations and normal self‐constituents. The multi‐subunit αβT‐cell receptor (TCR) operates outside of thermal equilibrium, harvesting energy via physical forces generated by T‐cell motility and actin‐myosin machinery. When a peptide‐bound major histocompatibility complex molecule (pMHC) on an antigen presenting cell is ligated, the αβTCR on the T cell leverages force to form a catch bond, prolonging bond lifetime, and enhancing antigen discrimination. Under load, the αβTCR undergoes reversible structural transitions involving partial unfolding of its clonotypic immunoglobulin‐like (Ig) domains and coupled rearrangements of associated CD3 subunits and structural elements. We postulate that transitions provide critical energy to initiate the signaling cascade via induction of αβTCR quaternary structural rearrangements, associated membrane perturbations, exposure of CD3 ITAMs to phosphorylation by non‐receptor tyrosine kinases, and phase separation of signaling molecules. Understanding force‐mediated signaling by the αβTCR clarifies long‐standing questions regarding αβTCR antigen recognition, specificity and affinity, providing a basis for continued investigation. Future directions include examining atomistic mechanisms of αβTCR signal initiation, performance quality, tissue compliance adaptability, and T‐cell memory fate. The mechanotransduction paradigm will foster improved rational design of T‐cell based vaccines, CAR‐Ts, and adoptive therapies.

Immunology↗
DOE OSTI2025

Roles for epigenetics in wood formation and stress response intrees–from basic biology to forest management

Annual model and crop species have been the subject of most epigenetic studies for plants. In contrast to annuals, forest trees persist on natural landscapes and experience environmental variation within and across seasons, years, and decades or even centuries. Most forest trees species are undomesticated and typically grown on variable landscapes with no irrigation or application of agricultural chemicals. Forest trees must thus rely on their inherent ability to alter growth and physiology to mitigate the effects of changing abiotic and biotic stressors. Like other plants, trees have mechanisms encoded in their genomic DNA sequence that can respond directly to stress events such as drought or heat. Hypothetically, it would be highly advantageous to join these mechanisms with a dynamic “memory” of past exposure to stress. It is now well established that annual model and crop plants can establish epigenetic-based memory of stress events that support more rapid and robust response to stress in the future. Here, evidence is discussed for epigenetic regulation and “memory” in two fundamental biological processes in trees, wood formation and abiotic stress response. Wood formation is an ideal trait for epigenetic research in trees, as wood formation is highly responsive to environmental conditions and includes multiple rapid developmental changes as cells adopt distinct fates within complex tissues. This is followed by a discussion of research needs that would provide the foundation for new epigenetic applications for forestry.

Groover, Andrew↗
DOE OSTI2025

Insights into regulatory T-cell and type-I interferon roles in determining abacavir-induced hypersensitivity or immune tolerance

Introduction Clinical use of several small molecule drugs may lead to severe T-cell-mediated idiosyncratic drug hypersensitivity reactions (iDHR) linked to HLA alleles, including abacavir (ABC) with HLA-B*57:01. Due to study limitations in humans, pathogenic networks in iDHR remain elusive. HLA transgenic murine models have been proposed to bridge knowledge gaps in tolerance and susceptibility to drugs. Methods Mice expressing HLA-B*57:01 and Foxp3-DTR/EGFP were generated to selectively deplete regulatory T-cells (Treg) with diphtheria toxin. ABC was administered for 8 days alone or together with cell- and cytokine-depleting antibodies. Cellular and transcriptomic responses were analyzed by RNA, flow cytometry and fluorescence methods. Results While CD8 + T-cell responses to ABC require HLA presentation, ABC also triggered mitochondrial stress in macrophagesin vitro, independently of HLA.In vivo, Treg were the primary mechanism of drug tolerance controlling HLA presentation and costimulation by antigen presenting cells. Treg ablation uncovered immune adverse events linked to activation and proliferation of both drug-specific and bystander CD8 + T-cells through CD28-mediated pathways with support from CD4 + non-Treg. Type-I interferon (IFN-I) and cellular-stress pathways influenced the fate of lymph node cells responding to ABC, implicating innate immune cells such as macrophages and plasmacytoid dendritic cells in the development of T-cell responses against the drug. IFN-I and IL-2 were necessary for CD8 + T-cell differentiation and ABC-induced adverse reactions. Conclusions This study unveils novel immune mechanisms driven by drug and host-related factors required forin vivoreactions and sheds light on potential biomarker and therapeutic targets for managing and preventing severe and life-threatening iDHR.

Immunology↗
DOE OSTI2025

Spatially structured bacterial interactions alter algal carbon flow to bacteria

Phytoplankton account for nearly half of global photosynthetic carbon fixation, and the fate of that carbon is regulated in large part by microbial food web processing. We currently lack a mechanistic understanding of how interactions among heterotrophic bacteria impact the fate of photosynthetically fixed carbon. Here, we used a set of bacterial isolates capable of growing on exudates from the diatom Phaeodactylum tricornutum to investigate how bacteria-bacteria interactions affect the balance between exudate remineralization and incorporation into biomass. With exometabolomics and genome-scale metabolic modeling, we estimated the degree of resource competition between bacterial pairs. In a sequential spent media experiment, we found that pairwise interactions were more beneficial than predicted based on resource competition alone, and 30% exhibited facilitative interactions. To link this to carbon fate, we used single-cell isotope tracing in a custom cultivation system to compare the impact of different "primary" bacterial strains in close proximity to live P. tricornutum on a distal "secondary" strain. We found that a primary strain with a high degree of competition decreased secondary strain carbon drawdown by 51% at the single-cell level, providing a quantitative metric for the "cost" of competition on algal carbon fate. Additionally, a primary strain classified as facilitative based on sequential interactions increased total algal-derived carbon assimilation by 7.6 times, integrated over all members, compared to the competitive primary strain. Our findings suggest that the degree of interaction between bacteria along a spectrum from competitive to facilitative is directly linked to algal carbon drawdown.

genome-scale metabolic model↗
DOE OSTI2025

Engineered Endosymbionts that Modulate Primary Macrophage Function and Attenuate Tumor Growth by Shifting the Tumor Microenvironment

Modulating gene expression in macrophages can be used to improve tissue regeneration and redirect tumor microenvironments (TMEs) toward positive therapeutic outcomes. We have developed Bacillus subtilis as an engineered endosymbiont (EES) capable of residing inside the eukaryotic host cell cytoplasm and controlling the fate of macrophages. Secretion of mammalian transcription factors (TFs) from B. subtilis that expresses listeriolysin O (LLO; allowing the EES to escape destruction by the macrophage) modulated expression of surface markers, cytokines, and chemokines, indicating functional changes in a macrophage/monocyte cell line. The engineered B. subtilis LLO TF strains were evaluated in murine bone marrow-derived macrophages (BMDMs) by flow cytometry, chemokine/cytokine profiling, metabolic assays, and RNA-Seq delivery of TFs by the EES shifted BMDM gene expression, production of cytokine and chemokines, and metabolic patterns, indicating that the TF strains could guide primary macrophage function. Thereafter, the ability of the TF strains to alter the TME was characterized in vivo in an orthotopic murine model of triple-negative breast cancer to assess therapeutic effects. The TF strains altered the TME by shifting immune cell composition and attenuating tumor growth. Additionally, multiple doses of the TF strains were well-tolerated by the mice. The use of B. subtilis LLO TF strains as EES showed promise as a unique cancer immunotherapy by directing the immune function intracellularly. The uses of EES could be expanded to modulate other mammalian cells over a range of biomedical applications.

60 APPLIED LIFE SCIENCES↗