Biology subjects

Wang, M. C.

Publications and source records attributed to Wang, M. C..

At least 19 recordsLinked to original sources

bioRxiv2026

Therapeutic acute intermittent hypoxia does not alter whole-brain cerebrovascular function in healthy individuals

Acute intermittent hypoxia (AIH) therapy is a promising intervention known to elicit beneficial neuroplasticity. It has been suggested that AIH may also modulate cerebrovascular function, yet the cerebrovascular effects of specific therapeutic intermittent hypoxia protocols remain poorly characterized. Understanding whether AIH results in favorable or adverse cerebrovascular changes is critical in establishing the safety of AIH treatments in populations with elevated cerebrovascular risk. This study investigated cerebral blood flow, cerebrovascular reactivity to hypoxia, and blood pressure effects in a sham-controlled crossover trial (NCT05164705). Healthy young adults (n=18) completed three-week arms of AIH (12 sessions, 15 cycles of 60 seconds hypoxia alternated with 60 seconds normoxia) and sham (6 sessions, normoxia) treatments; phase-contrast and arterial spin labeling magnetic resonance imaging were used to quantify whole-brain and regional cerebral blood flow and hypoxic cerebrovascular reactivity. Blood pressure was measured acutely (before and after each intervention session) and longitudinally (before and after 3 weeks of treatment). AIH treatment did not significantly alter whole-brain resting cerebral blood flow or cerebrovascular reactivity to hypoxia. Blood pressure was unaffected by the treatment acutely or longitudinally. Voxel-wise analysis identified modest regional perfusion increases in the frontal pole, postcentral gyri, and precentral gyri with AIH relative to sham. Significant variability between subjects and between sessions in the hypoxic burden delivered with this AIH protocol was also identified. Overall, this three-week therapeutic AIH protocol produced minimal sustained hemodynamic changes in healthy young adults. The insights from this trial lay a foundation for safely expanding access to this promising rehabilitative intervention in clinical populations.

physiology↗

bioRxiv2026

Organelle Volume Facilitates Spindle Positioning During C. elegans Female Meiosis

Cortical positioning of oocyte meiotic spindles is required for reducing chromosome number by segregating chromosomes into polar bodies. In C. elegans, kinesin-1 transports membrane-bound organelles inward into a central ball that is hypothesized to push the meiotic spindle outward. Using focused ion beam scanning electron microscopy, we found that the percent volume occupied by membrane-bound organelles was 28% in a mature oocyte that has completed endocytosis of the yolk precursor, vitellogenin, compared to 17% in a less mature oocyte that has not yet endocytosed vitellogenin. We therefore hypothesized that blocking endocytosis of vitellogenin would reduce the size of the central ball of organelles packed inward by kinesin-1 and limit outward movement of the spindle. Depletion of vitellogenin or proteins required for endocytosis resulted in a smaller central volume of kinesin-coated organelles and defective spindle positioning. A computer simulation of a simple exclusion model faithfully recapitulated wildtype and mutant spindle position phenotypes. These results support a volume exclusion model for positioning acentriolar meiotic spindles.

cell biology↗

bioRxiv2026

Comparative proteomic quantification reveals novel longevity regulators

Proteomics is a powerful tool for profiling the protein landscape underlying cellular and physiological processes. Advances in mass spectrometry-based methods, such as tandem-mass-tags (TMT) isobaric labeling-based proteomics at both MS2 and MS3, label-free quantification (LFQ) with data-dependent-acquisition (DDA) or data-independent acquisition (DIA)-based proteomics, and stable isotope labeling with amino acid (SILAC) spike-in-assisted proteomics, enable quantitative proteome comparisons across biological conditions. These five quantitative proteomic methods offer distinct advantages in coverage, throughput, and quantitative reproducibility. Here, we treated them as orthogonal approaches, retaining protein candidates with significant, consistent-direction changes supported across multiple independently instrumented methods to identify high-confidence protein-level changes associated with longevity. Insulin/insulin-like growth factor signaling (IIS) is a highly conserved longevity regulatory pathway from Caenorhabditis elegans to humans. By quantitatively profiling IIS mutants in C. elegans and performing genetic screening, we obtained a systems-view of proteomic changes linked to longevity and identified new longevity regulators. This systematic cross-method comparison also serves as a valuable resource for guiding the selection of quantitative proteomics approaches.

molecular biology↗

bioRxiv2026

Reconstituting Mouse Embryogenesis Ex Utero from Gastrulation to Fetal Development Reveals Maternally Independent Metabolic Programs

Mammalian development takes place inside the maternal uterus, creating technological constraints that make difficult the study of embryogenesis in live developing embryos. A central challenge for understanding the role of metabolism in mammalian development is discriminating placental and uterine-regulated signals from embryo-intrinsic processes independent of maternal influence, a process that until now has remained inseparable during gastrulation and organogenesis1-3. Ex utero culture systems allowing continuous growth of embryos during pre-gastrulation to organogenesis4,5 offer a promising solution to this challenge. Here, we present optimized ex utero culture platforms that support faithful development of mouse embryos from gastrulation (embryonic day 6.5/7.5) through the fetal period (embryonic day [~]12.5) and harnessed these platforms for dissecting metabolic transitions in vivo during embryogenesis independently of uterus and placenta. We characterized the metabolome of in utero and ex utero whole embryos, fetal organs and culture medium between embryonic days E6.5 and E12.5 by liquid chromatography mass-spectrometry (LC-MS) metabolomics, isotope tracing, and single cell transcriptomics. These datasets present a comprehensive overview of the dynamic embryonic metabolism during gastrulation and organogenesis in utero and ex utero. This analysis revealed that the midgestational metabolic switch occurring at E10.5-E11.5 is faithfully recapitulated ex utero, indicating that this transition is intrinsically programmed in embryonic tissues and does not require direct maternal or placental cues. Notably, oxygen availability modulated the extent of this transition, but elevated oxygen was insufficient to induce it prematurely, demonstrating that the switch is developmentally timed and only partially environmental-responsive. We further harnessed the ex utero platform for identifying and perturbing a mitochondrial redox shift at E7.5-E8.5 that is critical for developmental progress after gastrulation. These findings uncover the remarkable metabolic plasticity of the mammalian embryo, demonstrating its capacity to sustain growth independently of maternal inputs from the establishment of the body plan through the onset of the fetal period. Moreover, they highlight the use of long-term ex utero culture as a unique framework for dissecting the mechanisms that shape embryogenesis under physiological and experimentally perturbed conditions, while functionally uncoupling embryonic programs from maternal and placental influences.

developmental biology↗

bioRxiv2025

The fat-body secreted neuropeptide CCHa2 signals insulin-producing cells in the brain to promote sleep

Sleep is a fundamental behavior regulated by diverse environmental and physiological cues. While the central mechanisms underlying sleep regulation have been investigated in detail, far less is known about how nutrient signals from the periphery are communicated to the brain to modulate sleep. Here, we perform a targeted RNAi screen of genes enriched in the fat body and regulated by feeding state to identify genes that function in the fat body to regulate sleep in Drosophila. This analysis found that body-specific knockdown of CCHa2 significantly reduced sleep duration and sleep depth in fed flies, phenocopying sleep in starved flies. CCHa2-deficient flies exhibited reduced glycogen stores and diminished feeding drive. Analysis of single-cell transcriptomic atlases confirms that the CCHa2 receptor (CCHa2-R) is selectively expressed in Insulin Producing Cells (IPCs) of the fly brain. We find that knockdown of CCHa2-R in IPCs recapitulates the sleep loss phenotype of CCHa2 mutants, supporting a role in adipose-brain signaling. Further screening of genes identified in single cell atlases as being enriched in IPCs led to the identification of numerous genes that function in IPCs to regulate sleep including modulators of wnt and insulin signaling. Together, these findings identify a fat body-IPC axis that is a critical modulator of sleep duration and intensity.

neuroscience↗

bioRxiv2025

Form and function of actin impacts actin health and aging.

The actin cytoskeleton is a fundamental and highly conserved structure that functions in diverse cellular processes, yet its direct contribution to organismal aging remains unclear. Here, we systematically interrogated how genetic and pharmacologic perturbations of actin structure and function influence lifespan and various hallmarks of aging in Caenorhabditis elegans. Whole-animal and tissue-specific knockdown of actin and key actin-binding proteins (ABPs) - arx-2 (Arp2/3), unc-60 (cofilin), and lev-11 (tropomyosin) - led to premature disruption of filament organization, reduced lifespan, and tissue-specific physiological defects. Bulk and single-nucleus RNA-sequencing revealed that ABP knockdowns elicited a strongly "aged" transcriptome. Actin dysfunction broadly exacerbated many age-associated phenotypes, including mitochondrial dysfunction, lipid dysregulation, loss of proteostasis, impaired autophagy, and intestinal barrier failure. Pharmacological destabilization with Latrunculin A mirrored genetic knockdowns, while mild stabilization with Jasplakinolide modestly extended lifespan, emphasizing that optimal and finely-tuned actin function is critical for healthy aging. Finally, analysis of human genome-wide association data revealed that common ACTB polymorphisms correlate with differences in age-related decline in gait speed, suggesting evolutionary conservation of actins role in healthy aging. Taken together, our results provide a comprehensive and publicly accessible resource that maps, for the first time, how actin integrity intersects with diverse aging pathways across tissues and scales. This descriptive framework is intended to enable future mechanistic discovery by offering a deep, unbiased dataset that can be integrated with emerging studies to define how actin dynamics contribute to aging.

cell biology↗

bioRxiv2025

In-situ glial cell-surface proteomics identifies pro-longevity factors in Drosophila

Much focus has shifted towards understanding how glial dysfunction contributes to age-related neurodegeneration due to the critical roles glial cells play in maintaining healthy brain function. Cell-cell interactions, which are largely mediated by cell-surface proteins, control many critical aspects of development and physiology; as such, dysregulation of glial cell-surface proteins in particular is hypothesized to play an important role in age-related neurodegeneration. However, it remains technically difficult to profile glial cell-surface proteins in intact brains. Here, we applied a cell-surface proteomic profiling method to glial cells from intact brains in Drosophila, which enabled us to fully profile cell-surface proteomes in-situ, preserving native cell-cell interactions that would otherwise be omitted using traditional proteomics methods. Applying this platform to young and old flies, we investigated how glial cell-surface proteomes change during aging. We identified candidate genes predicted to be involved in brain aging, including several associated with neural development and synapse wiring molecules not previously thought to be particularly active in glia. Through a functional genetic screen, we identified one surface protein, DIP-{beta}, which is down-regulated in old flies and can increase fly lifespan when overexpressed in adult glial cells. We further performed whole-head single-nucleus RNA-seq and revealed that DIP-{beta} overexpression mainly impacts glial and fat cells. We also found that glial DIP-{beta} overexpression was associated with improved cell-cell communication, which may contribute to the observed lifespan extension. Our study is the first to apply in-situ cell-surface proteomics to glial cells in Drosophila, and to identify DIP-{beta} as a potential glial regulator of brain aging.

neuroscience↗

bioRxiv2025

Lysosomes Signal through Epigenome to Regulate Longevity across Generations

Epigenome is sensitive to metabolic inputs and crucial for aging. Lysosomes emerge as a signaling hub to sense metabolic cues and regulate longevity. We unveil that lysosomal metabolic pathways signal through the epigenome to regulate transgenerational longevity in Caenorhabditis elegans. We discovered that the induction of lysosomal lipid signaling and lysosomal AMP-activated protein kinase (AMPK), or the reduction of lysosomal mechanistic-target-of-rapamycin (mTOR) signaling, increases the expression of histone H3.3 variant and elevates H3K79 methylation, leading to lifespan extension across multiple generations. This transgenerational pro-longevity effect requires intestine-to-germline transportation of H3.3 and a germline-specific H3K79 methyltransferase, and can be recapitulated by overexpressing H3.3 or the H3K79 methyltransferase. This work uncovers a lysosome-epigenome signaling axis linking soma and germline to mediate the transgenerational inheritance of longevity.

genetics↗

bioRxiv2025

TEMI: Tissue Expansion Mass Spectrometry Imaging

The spatial distribution of diverse biomolecules in multicellular organisms is essential for their physiological functions. High-throughput in situ mapping of biomolecules is crucial for both basic and medical research, and requires high scanning speed, spatial resolution, and chemical sensitivity. Here, we developed a Tissue Expansion method compatible with matrix-assisted laser desorption/ionization Mass spectrometry Imaging (TEMI). TEMI reaches single-cell spatial resolution without sacrificing voxel throughput and enables the profiling of hundreds of biomolecules, including lipids, metabolites, peptides (proteins), and N-glycans. Using TEMI, we mapped the spatial distribution of biomolecules across various mammalian tissues and uncovered metabolic heterogeneity in tumors. TEMI can be easily adapted and broadly applied in biological and medical research, to advance spatial multi-omics profiling.

molecular biology↗

bioRxiv2024

Functional Dichotomy of Orbitofrontal Cortex and Anterior Cingulate Cortex Subregions in Decision-Making and Brain-Body Regulation

Mood disorders are associated with complex disruptions in brain networks, including those associated with the orbitofrontal cortex (OFC) and pregenual anterior cingulate cortex (pACC). The functional contribution of the caudal OFC (cOFC) has remained largely unexplored. We investigated the functions of the cOFC and pACC in macaques performing an approach-avoidance task by the combination of multimodal recordings and electrical microstimulation (EMS) of the cOFC. We assessed neural, autonomic and behavioral responses. We found the cOFC to be sensitive to both positive and negative stimuli, whereas the pACC was singificantly more active during aversive outcomes. EMS of the cOFC increased avoidance behavior, suggesting a causal role for the OFC subdivision in cost-benefit decision-making. Physiological measurements were positively correlated with behavioral patterns, emphasizing body-brain synchronization during emotionally significant decision-making. We suggest that the cOFC contributes to inducing pessimistic states, thereby making its dysfunction a potential contributor to the etiology of mood disorders.

neuroscience↗

bioRxiv2024

Variable Cerebral Blood Flow Responsiveness to Acute Hypoxic Hypoxia

Cerebrovascular reactivity (CVR) to changes in blood carbon dioxide and oxygen levels is a robust indicator of vascular health. Although CVR is typically assessed with hypercapnia, the interplay between carbon dioxide and oxygen, and their ultimate roles in dictating vascular tone, can vary with pathology. Methods to characterize vasoreactivity to oxygen changes, particularly hypoxia, would provide important complementary information to established hypercapnia techniques. However, existing methods to study hypoxic CVR, typically with arterial spin labeling (ASL) MRI, demonstrate high variability and paradoxical responses. To understand whether these responses are real or due to methodological confounds of ASL, we used phase-contrast MRI to quantify whole-brain blood flow in 21 participants during baseline, hypoxic, and hypercapnic respiratory states in three scan sessions. Hypoxic CVR reliability was poor-to-moderate (ICC=0.42 for CVR relative to PETO2 changes, ICC=0.56 relative to SpO2 changes) and was less reliable than hypercapnic CVR (ICC=0.67). Without the uncertainty from ASL-related confounds, we still observed paradoxical responses at each timepoint. Concurrent changes in blood carbon dioxide levels did not account for paradoxical responses. Hypoxic CVR and hypercapnic CVR shared approximately 40% of variance across the dataset, indicating that the two effects may indeed reflect distinct, complementary elements of vascular regulation.

neuroscience↗

bioRxiv2024

Chemical Induction of Longevity-Promoting Colanic Acid in the Host's Microbiota

Microbiota-derived metabolites have emerged as key regulators of longevity. The metabolic activity of the gut microbiota, influenced by dietary components and ingested chemical compounds, profoundly impacts host fitness. While the benefits of dietary prebiotics are well-known, chemically targeting the gut microbiota to enhance host fitness remains largely unexplored. Here, we report a novel chemical approach to induce a pro-longevity bacterial metabolite in the host gut. We discovered that specific Escherichia coli strains overproduce colanic acids (CAs) when exposed to a low dose of cephaloridine, leading to an increased lifespan in host Caenorhabditis elegans. In the mouse gut, oral administration of low-dose cephaloridine induces the transcription of the capsular biosynthesis operon responsible for CA biosynthesis in commensal E. coli, which overcomes the inhibition of CA biosynthesis above 30{degrees}C and enables its induction directly from the microbiota. Importantly, low-dose cephaloridine induces CA independently of its antibiotic properties through a previously unknown mechanism mediated by the membrane-bound histidine kinase ZraS. Our work lays the foundation for microbiota-based therapeutics through the chemical modulation of bacterial metabolism and reveals the promising potential of bacteria-targeting drugs in promoting host longevity.

developmental biology↗

bioRxiv2023

FITM2 deficiency results in ER lipid accumulation, ER stress, reduced apolipoprotein B lipidation, and VLDL triglyceride secretion in vitro and in mouse liver

Structured AbstractO_ST_ABSObjectivesC_ST_ABSTriglyceride (TG) association with apolipoprotein B100 (apoB100) serves to form very low density lipoproteins (VLDL) in the liver. The repertoire of factors that facilitate this association is incompletely defined. FITM2, an integral endoplasmic reticulum (ER) protein, was originally discovered as a factor participating in cytoplasmic lipid droplets (LDs) in tissues that do not form VLDL. We hypothesized that in the liver, in addition to promoting cytosolic LD formation, FITM2 would also transfer TG from its site of synthesis in the ER membrane to nascent VLDL particles within the ER lumen. MethodsExperiments were conducted using a rat hepatic cell line (McArdle-RH7777, or McA cells), an established model of mammalian lipoprotein metabolism, and mice. FITM2 expression was reduced using siRNA in cells and by liver specific cre-recombinase mediated deletion of the Fitm2 gene in mice. Effects of FITM2 deficiency on VLDL assembly and secretion in vitro and in vivo were measured by multiple methods, including density gradient ultracentrifugation, chromatography, mass spectrometry, simulated Raman spectroscopy (SRS) microscopy, sub-cellular fractionation, immunoprecipitation, immunofluorescence, and electron microscopy. Main findings1) FITM2-deficient hepatic cells in vitro and in vivo secrete TG-depleted VLDL particles, but the number of particles is unchanged compared to controls; 2) FITM2 deficiency in mice on a high fat diet (HFD) results in decreased plasma TG levels. The number of apoB100-containing lipoproteins remains similar, but shift from VLDL to LDL density; 3) Both in vitro and in vivo, when TG synthesis is stimulated and FITM2 is deficient, TG accumulates in the ER, and despite its availability this pool is unable to fully lipidate apoB100 particles; 4) FITM2 deficiency disrupts ER morphology and results in ER stress. Principal conclusionsThe results suggest that FITM2 contributes to VLDL lipidation, especially when newly synthesized hepatic TG is in abundance. In addition to its fundamental importance in VLDL assembly, the results also suggest that under dysmetabolic conditions, FITM2 may be a limiting factor that ultimately contributes to non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH).

biochemistry↗

bioRxiv2023

Quantitative Profiling of Lysosomal pH Heterogeneity using Fluorescence Lifetime Imaging Microscopy

Lysosomes play crucial roles in maintaining cellular homeostasis and promoting organism fitness. The pH of lysosomes is a crucial parameter for their proper function, and it is dynamically influenced by both intracellular and environmental factors. Here, we present a method based on fluorescence lifetime imaging microscopy (FLIM) for quantitatively analyzing lysosomal pH profiles in diverse types of primary mammalian cells and in different tissues of the live organism Caenorhabditis elegans. This FLIM-based method exhibits high sensitivity in resolving subtle pH differences, thereby revealing the heterogeneity of the lysosomal population within a cell and between cell types. The method enables rapid measurement of lysosomal pH changes in response to various environmental stimuli. Furthermore, the FLIM measurement of pH-sensitive dyes circumvents the need for transgenic reporters and mitigates potential confounding factors associated with varying dye concentrations or excitation light intensity. This FLIM approach offers absolute quantification of lysosomal pH and highlights the significance of lysosomal pH heterogeneity and dynamics, providing a valuable tool for studying lysosomal functions and their regulation in various physiological and pathological contexts.

cell biology↗

bioRxiv2023

Quantification of glutathione with high throughput live-cell imaging

Reduction oxidation (redox) reactions are central in life and altered redox state is associated with a spectrum of human diseases. Glutathione (GSH) is the most abundant antioxidant in eukaryotic cells and plays critical roles in maintaining redox homeostasis. Thus, measuring intracellular GSH level is an important method to assess the redox state of organism. The currently available GSH probes are based on irreversible chemical reactions with glutathione and cant monitor the real-time glutathione dynamics. Our group developed the first reversible reaction based fluorescent probe for glutathione, which can measure glutathione levels at high resolution using a confocal microscope and in the bulk scale with a flow cytometry. Most importantly it can quantitatively monitor the real-time GSH dynamics in living cells. Using the 2nd generation of GSH probe, RealThiol (RT), this study measured the GSH level in living Hela cells after treatment with varying concentrations of DL-Buthionine sulfoximine (BSO) which inhibits GSH synthesis, using a high throughput imaging system, Cytation 5 cell imaging reader. The results revealed that GSH probe RT at the concentration of 2.0 {micro}M accurately monitored the BSO treatment effect on GSH level in the Hela cells. The present results demonstrated that the GSH probe RT is sensitive and precise in GSH measurement in living cells at a high throughput imaging platform and has the potential to be applied to any cell lines.

biochemistry↗

bioRxiv2023

Contributions of attention to learning in multi-dimensional reward environments

Real-world choice options have many features or attributes, whereas the reward outcome from those options only depends on a few features/attributes. It has been shown that humans learn and combine feature-based with more complex conjunction-based learning to tackle challenges of learning in complex reward environments. However, it is unclear how different learning strategies interact to determine what features should be attended and control choice behavior, and how ensuing attention modulates future learning and/or choice. To address these questions, we examined human behavior during a three-dimensional learning task in which reward outcomes for different stimuli could be predicted based on a combination of an informative feature and conjunction. Using multiple approaches, we first confirmed that choice behavior and reward probabilities estimated by participants were best described by a model that learned the predictive values of both the informative feature and the informative conjunction. In this model, attention was controlled by the difference in these values in a cooperative manner such that attention depended on the integrated feature and conjunction values, and the resulting attention weights modulated learning by increasing the learning rate on attended features and conjunctions. However, there was little effect of attention on decision making. These results suggest that in multidimensional environments, humans direct their attention not only to selectively process reward-predictive attributes, but also to find parsimonious representations of the reward contingencies for more efficient learning. Significance StatementFrom trying exotic recipes to befriending new social groups, outcomes of real-life actions depend on many factors, but how do we learn the predictive values of those factors based on feedback we receive? It has been shown that humans simplify this problem by focusing on individual factors that are most predictive of the outcomes but can extend their learning strategy to include combinations of factors when necessary. Here, we examined interaction between attention and learning in a multidimensional reward environment that requires learning about individual features and their conjunctions. Using multiple approaches, we found that learning about features and conjunctions control attention in a cooperative manner and that the ensuing attention mainly modulates future learning and not decision making.

neuroscience↗

bioRxiv2023

Mitochondrial GTP Metabolism Regulates Reproductive Aging

Healthy mitochondria are critical for reproduction. During aging, both reproductive fitness and mitochondrial homeostasis decline. Mitochondrial metabolism and dynamics are key factors in supporting mitochondrial homeostasis. However, how they are coupled to control reproductive health remains unclear. We report that mitochondrial GTP metabolism acts through mitochondrial dynamics factors to regulate reproductive aging. We discovered that germline-only inactivation of GTP- but not ATP-specific succinyl-CoA synthetase (SCS), promotes reproductive longevity in Caenorhabditis elegans. We further revealed an age-associated increase in mitochondrial clustering surrounding oocyte nuclei, which is attenuated by the GTP-specific SCS inactivation. Germline-only induction of mitochondrial fission factors sufficiently promotes mitochondrial dispersion and reproductive longevity. Moreover, we discovered that bacterial inputs affect mitochondrial GTP and dynamics factors to modulate reproductive aging. These results demonstrate the significance of mitochondrial GTP metabolism in regulating oocyte mitochondrial homeostasis and reproductive longevity and reveal mitochondrial fission induction as an effective strategy to improve reproductive health.

cell biology↗

bioRxiv2023

Aging Atlas Reveals Cell-Type-Specific Regulation of Pro-longevity Strategies

Organism aging occurs at the multicellular level; however, how pro-longevity mechanisms slow down aging in different cell types remains unclear. We generated single-cell transcriptomic atlases across the lifespan of Caenorhabditis elegans under different pro-longevity conditions (http://mengwanglab.org/atlas). We found cell-specific, age-related changes across somatic and germ cell types and developed transcriptomic aging clocks for different tissues. These clocks enabled us to determine tissue-specific aging-slowing effects of different pro-longevity mechanisms, and identify major cell types sensitive to these regulations. Additionally, we provided a systemic view of alternative polyadenylation events in different cell types, as well as their cell-type-specific changes during aging and under different pro-longevity conditions. Together, this study provides molecular insights into how aging occurs in different cell types and how they respond to pro-longevity strategies.

developmental biology↗