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Murphy, C. T.

Publications and source records attributed to Murphy, C. T..

At least 19 recordsLinked to original sources

Glial cells gate small RNA transport from germline to brain during transgenerational epigenetic inheritance of behavior

How circulating RNAs reach their target tissue is not well understood. In C. elegans, small RNA signals that convey exposure to pathogenic Pseudomonas travel from the intestine to germline to neurons, allowing both learned pathogen avoidance and the transgenerational inheritance of this information for four generations, but how this Cer1 retrotransposon-bound RNA signal reaches the nervous system was previously unknown. We found that the RNA transporter SID-1, long thought to act in the intestine or germline, instead functions in a single cell type, the amphid sheath glia, where it is necessary and sufficient for learned avoidance. SID-1 mediates uptake of germline-derived RNA, followed by transcytosis to a neighboring sensory neuron, where the P11 target gene maco-1 is silenced. This glial "filter", which uses highly conserved molecular components to transcytose RNAs to neurons, reveals a general mechanism for gating small RNA access to the nervous system, paralleling the mammalian blood-brain barrier.

genetics↗

Pharmacologic AMPK Activation Extends Lifespan in C. elegans and Improves Aspects of Healthspan in Mice

Dysregulated energy metabolism is a hallmark of aging. Many interventions that extend lifespan converge on the conserved master regulator of energy metabolism, AMP-activated kinase (AMPK), and direct genetic activation of AMPK extends lifespan in multiple species. Here, we test the ability of a specific and potent pharmacologic AMPK activator, MK-8722, to extend lifespan in C. elegans and improve healthspan in aged mice. Treatment with MK-8722 from adulthood significantly extended lifespan in an AMPK-dependent manner in both wildtype and Cockayne syndrome model csb-1 mutant C. elegans, without impairing motility or reproductive capacity. Mice treated with MK-8722 from 18 until 24 months of age had significantly reduced body fat accumulation, blocked age-associated declines in fasting blood glucose and enhanced circadian rhythmicity in respiratory quotient, suggesting an improved overall metabolic state. Hepatic RNA sequencing revealed a decrease in inflammation-related pathways and an increase in sterol metabolic pathways, which was consistent with significantly increased levels of multiple sterol-derived metabolites, including lithocholic acid, a proposed mediator of the benefits of caloric restriction. Our results support pharmacologic AMPK activation as a promising gerotherapeutic strategy.

physiology↗

Caenorhabditis elegans avoids Todstoff, a novel nociceptive necrotaxis cue

To survive in hazardous environments, organisms must navigate and avoid myriad threats. Many species across phyla detect warning cues in the remains of dead or injured conspecifics, allowing them to enact defensive strategies and avoid a similar fate. Here, we demonstrate that Caenorhabditis elegans senses a novel aversive cue (which we term Todstoff, or death substance) present in the remains of dead worms that induces living conspecifics to perform negative necrotaxis behaviors. Todstoff is distinct from previously-identified social signals in C. elegans, including ascaroside and alarm pheromones, and our biochemical analysis has revealed that Todstoff may be a protein-associated amino acid derivative less than 1.35 kDa in size. We determined that Todstoff is sensed by the ASH polymodal nociceptive neurons, and further, that the necrotaxis signal is transduced via the activity of G-protein coupled receptor (GPCR) signaling, the Gi/o-like protein ODR-3, TRPV channels OSM-9 and OCR-2, and glutamatergic synaptic transmission to downstream AIB interneurons. Taken together, our work illuminates a post-mortem inter-animal chemical signaling pathway that promotes death avoidance, and thus, survival.

genetics↗

Exposure to deceased remains of conspecifics extends the lifespan of young and aged C. elegans via distinct pathways

Signaling factors, both external from an organisms environment and produced internally by its tissues, regulate the rate of aging. Loss of beneficial signals drives systemic aging, and conversely, restoring these youth-associated signals can rejuvenate an aging individual, as demonstrated by heterochronic parabiosis. Finding factors that promote organismal health and longevity therefore holds great therapeutic promise to slow aging and age-associated disease. Here, we report that exposure to the lysed remains of other worms extends C. elegans lifespan. This lifespan extension is not mediated by ascaroside pheromones and is not induced by bacterial cell lysate, suggesting that this effect is not merely produced by nutritional supplementation of cellular contents. We found that a period of discrete exposure at any point across the lifespan is sufficient to induce longevity. However, distinct pathways were activated in young and aged recipients; we found that lysate factors act through insulin/insulin-like growth factor/FOXO signaling (IIS) in young worms, while IIS-independent pathways extend lifespan in older worms. Using fluorescent gene reporter lines, we provide evidence that intestinal IIS is not activated in young worms, suggesting that lysate signals promote longevity via non-intestinal tissues. Our work identifies a novel longevity paradigm in which the remains of deceased C. elegans extend the lifespans of living conspecifics through multiple parallel pathways.

genetics↗

Controlled Release of Poly(U) via Acetalated Dextran Microparticles for Enhanced Vaccine Adjuvant Delivery

Diverse drug delivery systems are needed to address challenges in delivering novel vaccine components and enhancing their efficacy. Poly(U) is a single-stranded RNA composed of uracil repeats that acts as a toll-like receptor (TLR) 7/8 agonist, stimulating the innate immune system. However, poly(U) is susceptible to ribonuclease degradation without a delivery carrier, and its negative charge hinders cellular uptake. Encapsulation in acetalated dextran (Ace-DEX), a pH-sensitive, biodegradable polymer, addresses these challenges. This study encapsulated poly(U) into Ace-DEX Microparticles (MPs) with either spherical (smooth MPs) or collapsed-surface (wrinkled MPs) via spray-drying. It was hypothesized that the different morphologies of MPs would influence the vaccine efficacy after in vitro and in vivo models. Smooth poly(U) MPs had a higher percent viability and cytokine response in dendritic cells (DCs) than wrinkled poly(U) MPs. Moreover, mice vaccinated with smooth poly(U) MPs + ovalbumin (OVA) showed enhanced IL-2 production and IFN-{gamma} in response to OVA peptide and MHC-I immunodominant peptide restimulation, respectively, compared to wrinkled poly(U) MPs. However, mice vaccinated with wrinkled poly(U) MPs + OVA significantly increased B-cell and germinal center B-cell frequencies compared to mice vaccinated with phosphate buffered saline (PBS) whereas mice vaccinated with smooth poly(U) MPs + OVA did not. Overall, these findings suggest that smooth poly(U) MPs modulated dendritic cells and T-cells, and wrinkled poly(U) MPs modulated B-cells. Understanding how morphology influences these cell types will aid in optimizing future vaccine systems for more specific cellular targeting.

bioengineering↗

Molecular Requirements for C. elegans Transgenerational Epigenetic Inheritance of Pathogen Avoidance

C. elegans major food source is bacteria, and worms are naturally attracted to many bacterial species, including pathogenic Pseudomonas; in fact, worms prefer PA14 as well as wild bacteria over the lab E. coli strain (OP50) standardly used in the laboratory setting. Many labs have shown that despite this natural attraction to PA14, prior exposure to PA14 causes the worms to instead avoid PA14. This behavioral switch can happen on a relatively fast time scale, even within the duration of the choice assay. Here we show that accurate assessment of the animals true first choice requires the use of a paralytic (azide) to trap the worms at their initial choice, and to prevent the switch from attraction to avoidance of PA14 within the assay period. We previously discovered that exposure of C. elegans to 25{degrees}C plate-grown PA14 at 20{degrees}C for 24hrs not only leads to these animals switching from attraction to avoidance of PA14, but also to their progeny avoiding PA14 in the naive state, and this avoidance persists through the F4 generation. Other types of PA14 training can also cause P0 and/or F1 avoidance, but do not induce transgenerational (F2 and beyond) inheritance. We also previously showed that the transgenerational (P0-F4) learned avoidance is mediated by P11, a small RNA produced by PA14. P11 is both necessary and sufficient for transgenerational epigenetic inheritance of avoidance behavior. P11 is highly expressed in our standard growth conditions (25{degrees}C on surfaces), but not in other conditions, suggesting that reported failure to observe F2-F4 avoidance is most likely due to the absence of P11 expression in PA14 in the experimenters growth conditions. Through mutant analyses, we have tested many genes - including germline regulators, small RNA uptake, RNA interference/processing, chromatin modifiers, and neuronal genes -for their involvement in transgenerational inheritance of learned pathogen avoidance, allowing us to better understand the molecular requirements for this process. We previously found that wild C. elegans strains also show TEI of learned pathogen avoidance, and that at least two other wild bacteria, P. vranovensis and P. fluorescens 15, induce this transgenerational avoidance. The avoidance induced by each Pseudomonas species functions through a specific, distinct small RNA (Pv1 in P. vranovensis and Pfs1 in P. fluorescens 15, respectively) that either directly or indirectly reduce the levels of the gene maco-1, which in turn regulates daf-7 expression in the ASI neuron and subsequent avoidance behavior. The conservation of multiple components of this small RNA TEI mechanism across C. elegans strains and in multiple Pseudomonas species suggests that this transgenerational learned avoidance behavior is likely to be functional and physiologically important in wild conditions.

genetics↗

Male-specific features of C. elegans neuronal aging

Aging is a complex biological process, with sexually dimorphic aspects. For example, men and women differ in their vulnerabilities in cognitive decline, suggesting biological sex may contribute to the heterogeneous nature of aging. Although we know a great deal about the cognitive aging of hermaphrodites of the model system C. elegans, less is known about cognitive decline in males. Through behavioral analyses, we found that the cognitive aging process has both sex-shared and sex-dimorphic characteristics. Through neuron-specific sequencing, we identified neuronal age-associated sex-differential targets. In addition to sex-shared neuronal aging genes, males differentially downregulate mitochondrial metabolic genes and upregulate GPCR genes with age. In addition, the X chromosome exhibits increased gene expression in hermaphrodites and altered dosage compensation complex expression with age, indicating possible X-chromosomal dysregulation that contributes to sexual dimorphism in cognitive aging. Finally, we found that the sex-differentially expressed gene hrg-7, which encodes an aspartic-type endopeptidase, regulates male behavior during cognitive aging but does not affect hermaphrodites behaviors. Overall, these results suggest that males and hermaphrodites exhibit different age-related neuronal changes. This study will strengthen our understanding of sex-specific vulnerability and resilience and help identify new pathways to target with novel treatments that could benefit both sexes.

neuroscience↗

A small RNA from a natural bacterial pathogen of C. elegans induces transgenerational inheritance of learned avoidance

Previously, we discovered that a small RNA from a clinical isolate of Pseudomonas aeruginosa, PA14, induces learned avoidance and its transgenerational inheritance in C. elegans. Pseudomonas aeruginosa is an important human pathogen, and there are other Pseudomonads in C. elegans natural habitat, but it is unclear whether C. elegans ever encounters PA14-like bacteria in the wild. Thus, it is not known if small RNAs from bacteria found in C. elegans natural habitat can also regulate host behavior and produce heritable behavioral effects. Here we found that a pathogenic Pseudomonas vranovensis strain isolated from the C. elegans microbiota, GRb0427, like PA14, regulates worm behavior: worms learn to avoid this pathogenic bacterium following exposure to GRb0427, and this learned avoidance is inherited for four generations. The learned response is entirely mediated by bacterially-produced small RNAs, which induce avoidance and transgenerational inheritance, providing further support that such mechanisms of learning and inheritance exist in the wild. Using bacterial small RNA sequencing, we identified Pv1, a small RNA from GRb0427, that matches the sequence of C. elegans maco-1. We find that Pv1 is both necessary and sufficient to induce learned avoidance of Grb0427. However, Pv1 also results in avoidance of a beneficial microbiome strain, P. mendocina; this potentially maladaptive response may favor reversal of the transgenerational memory after a few generations. Our findings suggest that bacterial small RNA-mediated regulation of host behavior and its transgenerational inheritance are functional in C. elegans natural environment, and that different bacterial small RNA-mediated regulation systems evolved independently but define shared molecular features of bacterial small RNAs that produce transgenerationally-inherited effects.

genetics↗

Neuronal Activation of the Gαq Protein EGL-30/GNAQ Late in Life Rejuvenates Cognition Across Species

Cognitive decline is perhaps the most devastating aging loss. EGL-30/GNAQ and Gq signaling pathways are highly conserved between C. elegans and mammals. We find that activation of EGL-30 in aged worms at least triples memory span, and we wondered if this highly conserved pathway could also improve memory in very old mice. Murine Gnaq is enriched in hippocampal excitatory neurons and declines with age. Furthermore, GNAQ gain-of-function significantly improved memory in aged mice: GNAQ(gf) in hippocampal neurons of 24-month-old mice rescued age-related impairments in health metrics and long-term memory. Single-nucleus RNAseq revealed gene expression changes related to synaptic function, axon guidance, and learning and memory pathways. Several worm orthologs of mouse genes upregulated by GNAQ(gf) overexpression are required for EGL-30(gf)-dependent memory improvement. These results demonstrate that the molecular and genetic pathways between C. elegans and mammals are highly conserved, as activation of EGL-30/GNAQ, a pathway first identified in worms, rejuvenates cognitive function in two-year old mice (the equivalent of 70-80 yo humans). To our knowledge, this is the oldest age an intervention has successfully improved age-related cognitive decline. One-Sentence SummaryNeuronal activation of the Gq protein EGL-30/GNAQ restores long-term memory at old age in worms and mice.

neuroscience↗

Signaling from the C. elegans Hypodermis Non-autonomously Facilitates Short-term Associative Memory

Memory loss is one of the most debilitating symptoms of aging. While we normally think of memory regulation as autonomous to the brain, other factors outside of the brain can also affect neuron function. We have shown that the longevity insulin/IGF-1 signaling (IIS) pathway regulates neuron-specific activity, but whether the maintenance of memory through the IIS pathway is completely autonomous to the nervous system, or if there are systemic inputs, is unknown. We address this question using the auxin-inducible degradation (AID) system to degrade the IIS receptor, DAF-2, in specific tissues. Surprisingly, DAF-2 degradation specifically in the hypodermis improves memory in both young and aged C. elegans through the hypodermal expression of the diffusible Notch ligand, OSM-11. The Notch receptor LIN-12 is required for OSM-11s effect on memory, as are the downstream transcription factor LAG-1 and co-activator SEL-8. Furthermore, mid-life overexpression of the Notch ligand OSM-11 improves memory and slows cognitive decline. Hypodermal DAF-2 degradation suppresses the expression of ins-19, whose downregulation extends memory. Together, our data suggest a model in which the hypodermis, a metabolic tissue, can non-autonomously regulate neuronal activity and function, indicating a systemic connection between metabolism and memory regulation.

genetics↗

Enhanced Branched-Chain Amino Acid Metabolism Improves Age-related Reproductive Function

Reproductive aging is one of the earliest human aging phenotypes, and mitochondrial dysfunction has been linked to oocyte quality decline. However, it is not known which mitochondrial metabolic processes are critical for oocyte quality maintenance with age. To understand how mitochondrial processes contribute to C. elegans oocyte quality, we characterized the mitochondrial proteomes of young and aged wild-type and long-reproductive daf-2 mutants. Here we show that the mitochondrial proteomic profiles of young wild-type and daf-2 worms are similar and share upregulation of branched-chain amino acid (BCAA) metabolism pathway enzymes. Reduction of the BCAA catabolism enzyme BCAT-1 shortens reproduction, elevates mitochondrial reactive oxygen species levels, and shifts mitochondrial localization. Moreover, bcat-1 knockdown decreases oocyte quality in daf-2 worms and reduces reproductive capability, indicating the role of this pathway in the maintenance of oocyte quality with age. Importantly, oocyte quality deterioration can be delayed, and reproduction can be extended in wild-type animals both by bcat-1 overexpression and by supplementing with Vitamin B1, a cofactor needed for BCAA metabolism.

cell biology↗

CeLab, a Microfluidic Platform for the Study of Life History Traits, reveals Metformin and SGK-1 regulation of Longevity and Reproductive Span

The potential to carry out high-throughput assays in a whole organism in a small space is one of the benefits of C. elegans, but worm assays often require a large sample size with frequent physical manipulations, rendering them highly labor-intensive. Microfluidic assays have been designed with specific questions in mind, such as analysis of behavior, embryonic development, lifespan, and motility. While these devices have many advantages, current technologies to automate worm experiments have several limitations that prevent widespread adoption, and most do not allow analyses of reproduction-linked traits. We developed a miniature C. elegans lab-on-a-chip device, CeLab, a reusable, multi-layer device with 200 separate incubation arenas that allows progeny removal, to automate a variety of worm assays on both individual and population levels. CeLab enables high-throughput simultaneous analysis of lifespan, reproductive span, and progeny production, refuting assumptions about the Disposable Soma hypothesis. Because CeLab chambers require small volumes, the chip is ideal for drug screens; we found that drugs previously shown to increase lifespan also increase reproductive span, and we discovered that low-dose metformin increases both. CeLab reduces the limitations of escaping and matricide that typically limit plate assays, revealing that feeding with heat-killed bacteria greatly extends lifespan and reproductive span of mated animals. CeLab allows tracking of life history traits of individuals, which revealed that the nutrient-sensing mTOR pathway mutant, sgk-1, reproduces nearly until its death. These findings would not have been possible to make in standard plate assays, in low-throughput assays, or in normal population assays.

bioengineering↗

A systems biology-based identification and in vivo functional screening of Alzheimer's disease risk genes reveals modulators of memory function

Genome-wide association studies (GWAS) have uncovered over 40 genomic loci associated with risk for late-onset Alzheimers Disease (LOAD), but identification of the underlying causal genes remains challenging. While the role of glial biology in the mediation of LOAD genetic risk has been increasingly recognized, recent studies of induced pluripotent stem cell (iPSC)-derived neurons from LOAD patients have demonstrated the existence of neuronal cell-intrinsic functional defects, absent interactions with other brain cell types or exposure to neurotoxic insults. Here, we searched for genetic contributions to neuronal dysfunction in LOAD pathobiology, using an integrative systems approach that incorporated multi-evidence-based gene-mapping and network analysis-based prioritization. We found widespread dysfunction in neuronal gene co-expression networks in the LOAD brain and identified synaptic and endolysosomal function as being specifically impacted by LOAD-associated genetic variation. A systematic perturbation screening of candidate risk genes in C. elegans revealed that neuronal knockdown of the LOAD risk gene orthologs vha-10 (ATP6V1G2), cmd-1 (CALM3), amph-1 (BIN1), ephx-1 (NGEF), and pho-5 (ACP2) significantly alters short/intermediate-term memory function, the cognitive domain affected earliest during LOAD progression. These results highlight the impact of LOAD risk genes on evolutionarily conserved memory function, as mediated through neuronal endosomal dysfunction, and identify new targets for further mechanistic interrogation.

genetics↗

Fission and PINK-1-mediated mitophagy are required for Insulin/IGF-1 signaling mutant reproductive longevity

Womens reproductive cessation is the earliest sign of human aging and is caused by decreasing oocyte quality. Similarly, C. elegans reproduction declines with age and is caused by oocyte quality decline. Aberrant mitochondrial dynamics are a hallmark of age-related dysfunction, but the role of mitochondrial morphology in reproductive aging is largely unknown. We examined the requirements for mitochondrial fusion and fission in oocytes of both wild-type worms and the long-lived, long-reproducing insulin-like receptor mutant daf-2. We find that normal reproduction requires both fusion and fission. By contrast, daf-2 mutants require fission, but not fusion, for reproductive span extension. daf-2 mutant oocytes mitochondria are punctate (fissioned) and may be primed for mitophagy, as loss of the mitophagy regulator PINK-1 shortens daf-2s reproductive span. Our data suggest that daf-2 maintain oocyte mitochondria quality with age via a shift toward punctate mitochondrial morphology and mitophagy to extend reproductive longevity.

genetics↗

piRNAs regulate a Hedgehog germline-to-soma pro-aging signal

The reproductive system regulates the aging of the soma through competing anti- and pro-aging signals. Germline removal extends somatic lifespan through conserved pathways including Insulin, mTOR, and steroid signaling, while germline hyperactivity cuts lifespan short through mechanisms that remain elusive. Here, we show that mating-induced germline hyperactivity leads to the dramatic downregulation of piRNAs, which in turn releases silencing of their targets, including the Hedgehog-like ligand encoding genes wrt-1 and wrt-10, ultimately causing somatic collapse and early death. Germline-produced Hedgehog signals require PTR-6 and PTR-16 receptors for mating-induced body shrinking and lifespan shortening. Our results reveal an unconventional role of the piRNA pathway in transcriptional regulation of Hedgehog signaling, as well as a new role of Hedgehog signaling in the regulation of longevity and somatic maintenance. Our data suggest that Hedgehog signaling is controlled by the tunable piRNA pathway to encode the previously unknown germline-to-soma pro-aging signal. Mating-induced downregulation of piRNAs in the germline and subsequent signaling to the soma via the Hedgehog pathway enables the animal to tune its somatic resource allocation in response to germline needs to optimize reproductive timing and survival.

genetics↗

GAIT-GM integrative cross-omics analyses reveal cholinergic defects in a C. elegans model of Parkinson's disease

BackgroundParkinsons disease (PD) is a disabling neurodegenerative disorder in which multiple cell types, including dopaminergic and cholinergic neurons, are affected. The mechanisms of neurodegeneration in PD are unknown, limiting the development of therapies directed at disease-relevant molecular targets. C. elegans is a genetically tractable model system that can be used to disentangle disease mechanisms in complex diseases such as PD. Such mechanisms can be studied combining high-throughput molecular profiling technologies such as transcriptomics and metabolomics. However, the integrative analysis of multi-omics data in order to unravel disease mechanisms is a challenging task without advanced bioinformatics training. Galaxy, a widely-used resource for enabling bioinformatics analysis by the broad scientific community, has poor representation of multi-omics integration pipelines. ResultsWe present the integrative analysis of gene expression and metabolite levels of a C. elegans PD model using GAIT-GM, a new Galaxy tool for multi-omics data analysis. Using GAIT-GM, we discovered an association between branched-chain amino acid metabolism and cholinergic neurons in the C. elegans PD model. An independent follow-up experiment uncovered cholinergic neurodegeneration in the C. elegans model that is consistent with cholinergic cell loss observed in PD. ConclusionGAIT-GM is an easy to use Galaxy-based tool for generating novel testable hypotheses of disease mechanisms involving gene-metabolite relationships.

neuroscience↗

CeAid: A smartphone application for logging and plotting C. elegans assays

C. elegans is used as a model organism to study a wide range of topics in molecular and cellular biology. Conventional C. elegans assays often require a large sample size with frequent manipulations, rendering them labor-intensive. Automated high-throughput workflows may not be always the best solution to reduce benchwork labor, as they may introduce more complexity. Thus, most assays are carried out manually, where logging and digitizing experimental data can be as time-consuming as picking and scoring worms. Here we report the development of CeAid, C. elegans Application for inputting data, which significantly expedites the data entry process, utilizing swiping gestures and a voice recognition algorithm for logging data using a standard smartphone or Android device. This modular platform can also be adapted for a wide range of assays where recording data is laborious, even beyond worm research.

genetics↗

Horizontal and vertical transmission of transgenerational memories via the Cer1 transposon

Animals face both external and internal dangers: pathogens threaten from the environment, and unstable genomic elements threaten from within. Previously, we discovered that C. elegans protects itself from pathogens by "reading" bacterial small RNAs and using this information to both induce avoidance and transmit memories for several generations. Here we found that these memories can be transferred to naive animals via Cer1 retrotransposon-encoded capsids. Cer1 functions at the step of transmission of information from the germline to neurons, and is required for C. elegans learned avoidance ability and for mothers to pass this information on to progeny. The presence of the Cer1 retrotransposon in wild C. elegans strains correlates with the ability to learn and inherit small RNA-induced pathogen avoidance. Together, these results suggest that C. elegans has co-opted a potentially dangerous retrotransposon to instead protect itself and its progeny from a common pathogen through its inter-tissue signaling ability, hijacking this genomic element for its own adaptive immunity benefit.

genetics↗