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Title: A Caenorhabditis elegans Model of Age-dependent Neurodegeneration.
Creator: Jia, Kailiang, Graduate College
Abstract/Description: The probability of humans developing neurodegenerative diseases increases as one ages. So the purpose of this study is to use the nematode Caenorhabditis elegans as a genetic model for determining if they develop age-dependent neuronal changes.
Date Issued: 2014
PURL: http://purl.flvc.org/fau/fd/FA00005151
Format: Document (PDF)

Title: Antibiotic resistance in the oral bacterial community.
Creator: Famuyiwa, Toluleke, Esiobu, Nwadiuto, Jia, Kailiang, Graduate College
Abstract/Description: Purpose: This study was designed to define the antibiotic resistance index of the cultivable oral microbiome to Amoxiacilin Clavulanic acid, Vancomycin, Ciprofloxacin, Clarithomycin, Chlorotetracyclin, Bacitracin, Kanamycin and Tobramycin using a new method adapted from the Kirby Bauer assay. Method: Oral wash samples were collected from 2 current smokers and 2 nonsmokers. Bacterial community were pelleted by centrifugation and used to create a lawn for the assay employing standard disk...
Show morePurpose: This study was designed to define the antibiotic resistance index of the cultivable oral microbiome to Amoxiacilin Clavulanic acid, Vancomycin, Ciprofloxacin, Clarithomycin, Chlorotetracyclin, Bacitracin, Kanamycin and Tobramycin using a new method adapted from the Kirby Bauer assay. Method: Oral wash samples were collected from 2 current smokers and 2 nonsmokers. Bacterial community were pelleted by centrifugation and used to create a lawn for the assay employing standard disk diffusion assay. Zones of inhibition and number of colonies in the zone were recorded. Mean values of inhibition zones were compared to established databases to draw conclusions. Result: The zones of inhibition of Bacitracin antibiotics shows that several bacteria from one of the non smokers were resistant to Bacitracin, while the smokers showed marked susceptibility. Conclusion: The new method developed in our lab yielded consistent set of data which serve as criteria for determining resistance of the oral microbiome to antibiotics. Quite remarkably, it is known that pathogenic beta Streptococci are susceptible to Bacitracin while non-pathogens are not; confirming that healthy persons harbor the healthy strains of streptococci. However the unanswered question is …. Could these normal biota pick up genes and become resistant too? Only time and human habits will decide but we have developed a baseline and an easy method for testing.
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Date Issued: 2014
PURL: http://purl.flvc.org/fau/fd/FA00005814
Format: Document (PDF)

Title: Neuronal autophagy activity is essential for insulin growth factor signaling-regulated lifespan extension in C. elegans.
Creator: Minnerly, Justin, Jia, Kailiang, Zhang, Jiuli, Graduate College
Abstract/Description: The conserved insulin growth factor IGF signaling pathway is one of the major regulators of lifespan in many species including C. elegans. In C. elegans the insulin/IGF-like receptor is encoded by the daf-2 gene, mutations in which result in lifespan extension. The daf-2 activity in the nervous system controls these phenotypes cell nonautonomously. Interestingly, the longevity phenotype of daf-2 mutant worms is dependent on macroautophagy hereafter autophagy. Autophagy is a highly conserved...
Show moreThe conserved insulin growth factor IGF signaling pathway is one of the major regulators of lifespan in many species including C. elegans. In C. elegans the insulin/IGF-like receptor is encoded by the daf-2 gene, mutations in which result in lifespan extension. The daf-2 activity in the nervous system controls these phenotypes cell nonautonomously. Interestingly, the longevity phenotype of daf-2 mutant worms is dependent on macroautophagy hereafter autophagy. Autophagy is a highly conserved lysosomal degradation pathway involved in the removal of long-lived proteins and cytoplasmic organelles. During autophagy, cellular components are sequestered into the double-membrane autophagosomes and delivered to lysosomes for degradation. Increasing evidence has emerged that the autophagy process is a central regulator of lifespan that is required for the effects of DAF-2 signaling, dietary restriction and some mitochondrial mutations on C. elegans longevity. It is unknown however whether autophagy activity in every tissue or in a single tissue mediates the influence of these longevity signals. To address this question, we examined the tissue requirement of the autophagy gene atg-18 for the lifespan of wild type animals and the daf-2 mutant. We discovered that neurons and intestinal cells are two key tissues where atg-18 mediates the effect of DAF-2 insulin-like signaling on lifespan, suggesting autophagy acts cell nonautonomously in controlling C. elegans adult longevity. Moreover, we found that neuronal release of neuropeptides is required for the cell non-autonomous function of neuronal autophagy activity in controlling C. elegans lifespan.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00005900
Format: Document (PDF)

Title: The Role of Mitophagy in the Longevity of Caenorhabditis elegans.
Creator: Ochoa, Laura, Jia, Kailiang
Abstract/Description: FAU's Office of Undergraduate Research and Inquiry hosts an annual symposium where students engaged in undergraduate research may present their findings either through a poster presentation or an oral presentation.
Date Issued: 2011
PURL: http://purl.flvc.org/fau/fd/FA00005444
Format: Document (PDF)

Title: Identification of C. elegans ortholog of spinster.
Creator: Kobler, Patrick, Jia, Kailiang
Date Issued: 2013-04-05
PURL: http://purl.flvc.org/fcla/dt/3361106
Subject Headings: Autophagy, Lysosomal storage diseases, Caenorhabditis elegans
Format: Document (PDF)

Title: Tissue-specific requirement of the autophagy gene atg-18 in controlling C. elegans dauer morphogenesis, fat metabolism and adult longevity.
Creator: Minnerly, Justin, Zhang, Jiuli, Graduate College, Jia, Kailiang
Abstract/Description: The conserved insulin growth factor IGF signaling pathway is one of the major regulators of lifespan in many species including C. elegans. In C. elegans the insulin/IGF-like receptor is encoded by the daf-2 gene, mutations in which result in lifespan extension, fat accumulation and dauer formation. The daf-2 activity in the nervous system controls these phenotypes cell non-autonomously. Interestingly, the longevity phenotype of daf-2 mutant worms is dependent on macroautophagy hereafter...
Show moreThe conserved insulin growth factor IGF signaling pathway is one of the major regulators of lifespan in many species including C. elegans. In C. elegans the insulin/IGF-like receptor is encoded by the daf-2 gene, mutations in which result in lifespan extension, fat accumulation and dauer formation. The daf-2 activity in the nervous system controls these phenotypes cell non-autonomously. Interestingly, the longevity phenotype of daf-2 mutant worms is dependent on macroautophagy hereafter autophagy. Autophagy is a highly conserved lysosomal degradation pathway involved in the removal of long-lived proteins and cytoplasmic organelles. During autophagy, cellular components are sequestered into the double-membrane autophagosomes and delivered to lysosomes for degradation. Increasing evidence has emerged that the autophagy process is a central regulator of lifespan that is required for the effects of DAF-2 signaling, dietary restriction and some mitochondrial mutations on C. elegans longevity. It is unknown however whether autophagy activity in every tissue or in a single tissue mediates the influence of these longevity signals. To address this question, we examined the tissue requirement of autophagy gene atg-18 for the lifespan of wild type animals and the daf-2 mutant. We discovered that neurons and intestinal cells are two key tissues where atg-18 mediates the effect of DAF-2 insulin-like signaling on lifespan, fat accumulation and dauer morphogenesis, suggesting autophagy acts cell non-autonomously in controlling C. elegans dauer formation, fat metabolism and adult longevity.
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Date Issued: 2014
PURL: http://purl.flvc.org/fau/fd/FA00005160
Format: Document (PDF)

Title: Neuron- Specific Requirement of Autophagy Gene atg-18 for Lifespan and Dauer Morphogenesis of daf-2 Mutant C. elegans.
Creator: Phillips, Aileen, Jia, Kailiang, Harriet L. Wilkes Honors College
Abstract/Description: We recently discovered that autophagy, a conserved lysosomal degradation pathway, is necessary for increased lifespan and dauer morphogenesis of daf-2 mutant Caenorhabditis elegans. daf-2 encodes the worm orthologue of an insulin-like growth factor receptor. Moreover, we found neuronal autophagy activity is sufficient to fulfill this requirement. In this study we used the unc-42 promoter to express autophagy gene atg-18 in a subset of C. elegans neurons to examine whether autophagy activity...
Show moreWe recently discovered that autophagy, a conserved lysosomal degradation pathway, is necessary for increased lifespan and dauer morphogenesis of daf-2 mutant Caenorhabditis elegans. daf-2 encodes the worm orthologue of an insulin-like growth factor receptor. Moreover, we found neuronal autophagy activity is sufficient to fulfill this requirement. In this study we used the unc-42 promoter to express autophagy gene atg-18 in a subset of C. elegans neurons to examine whether autophagy activity in these neurons is sufficient to execute its function in extension of lifespan and completion of dauer morphogenesis in daf-2 mutants. Here we show expression of atg-18 in these ons fails to rescue the effect of atg-18 mutations on the longevity and dauer morphogenesis of daf-2 mutant worms, indicating that the requirement of neuronal autophagy in C. elegans for these effects is specific to neurons where unc-42 promoter is not active.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00003652
Format: Document (PDF)

Title: A Protocol to Infect Caenorhabditis elegans with Salmonella typhimuri.
Creator: Jiuli Zhang, Kailiang Jia
Abstract/Description: In the last decade, C. elegans has emerged as an invertebrate organism to study interactions between hosts and pathogens, including the host defense against gram-negative bacterium Salmonella typhimurium. Salmonella establishes persistent infection in the intestine of C. elegans and results in early death of infected animals. A number of immunity mechanisms have been identified in C. elegans to defend against Salmonella infections. Autophagy, an evolutionarily conserved lysosomal degradation...
Show moreIn the last decade, C. elegans has emerged as an invertebrate organism to study interactions between hosts and pathogens, including the host defense against gram-negative bacterium Salmonella typhimurium. Salmonella establishes persistent infection in the intestine of C. elegans and results in early death of infected animals. A number of immunity mechanisms have been identified in C. elegans to defend against Salmonella infections. Autophagy, an evolutionarily conserved lysosomal degradation pathway, has been shown to limit the Salmonella replication in C. elegans and in mammals. Here, a protocol is described to infect C. elegans with Salmonella typhimurium, in which the worms are exposed to Salmonella for a limited time, similar to Salmonella infection in humans. Salmonella infection significantly shortens the lifespan of C. elegans. Using the essential autophagy gene bec-1 as an example, we combined this infection method with C. elegans RNAi feeding approach and showed this protocol can be used to examine the function of C. elegans host genes in defense against Salmonella infection. Since C. elegans whole genome RNAi libraries are available, this protocol makes it possible to comprehensively screen for C. elegans genes that protect against Salmonella and other intestinal pathogens using genome-wide RNAi libraries.
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Date Issued: 2014
PURL: http://purl.flvc.org/fau/fd/FAUIR000528
Format: Document (PDF)

Title: The cell non-autonomous function of ATG-18 is essential for neuroendocrine regulation of Caenorhabditis elegans lifespan.
Creator: Justin Minnerly, Jiuli Zhang, Thomas Parker, Tiffany Kaul, Kailiang Jia
Abstract/Description: Restriction of dietary food without malnutrition robustly extends lifespan in more than twenty species. It was also reported that fruit flies (Drosophila melanogaster) deficient in olfactory function live longer and that the longevity induced by food restriction is partially due to decreased olfaction. These observations suggest food assimilation through the gastrointestinal tract and food smell detected by olfactory neurons influence lifespan. The insulin growth factor signaling pathway is...
Show moreRestriction of dietary food without malnutrition robustly extends lifespan in more than twenty species. It was also reported that fruit flies (Drosophila melanogaster) deficient in olfactory function live longer and that the longevity induced by food restriction is partially due to decreased olfaction. These observations suggest food assimilation through the gastrointestinal tract and food smell detected by olfactory neurons influence lifespan. The insulin growth factor signaling pathway is regulated by nutrient levels and has been shown to mediate the lifespan extension conferred by food restriction and defective gustatory neurons in the nematode Caenorhabditis elegans. However, the mechanism remains unclear. Autophagy is a lysosomal degradation pathway and is sensitive to nutrient availability. We found autophagy activity in the intestine and food sensory neurons acts in parallel to mediate food restriction and insulin signaling regulated lifespan extension in Caenorhabditis elegans. Moreover, intestinal and neuronal autophagy converge on unidentified neurons to control the secretion of neuropeptides that regulate lifespan. These data suggest autophagy is an essential component in a neuroendocrine pathway that coordinates how environmental food cues detected by sensory neurons and food nutrients assimilated by the intestine influence lifespan. These findings may contribute to understanding the aging process in mammals.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FAUIR000531
Format: Document (PDF)

Title: Intestinal autophagy activity is essential for host defense against Salmonella typhimurium infection in Caenorhabditis elega.
Creator: Alexander Curt, Jiuli Zhang, Justin Minnerly, Kailiang Jia
Abstract/Description: Salmonella typhimurium infects both intestinal epithelial cells and macrophages. Autophagy is a lysosomal degradation pathway that is present in all eukaryotes. Autophagy has been reported to limit the Salmonella replication in Caenorhabditis elegans and in mammals. However, it is unknown whether intestinal autophagy activity plays a role in host defense against Salmonella infection in C. elegans. In this study, we inhibited the autophagy gene bec-1 in different C. elegans tissues and...
Show moreSalmonella typhimurium infects both intestinal epithelial cells and macrophages. Autophagy is a lysosomal degradation pathway that is present in all eukaryotes. Autophagy has been reported to limit the Salmonella replication in Caenorhabditis elegans and in mammals. However, it is unknown whether intestinal autophagy activity plays a role in host defense against Salmonella infection in C. elegans. In this study, we inhibited the autophagy gene bec-1 in different C. elegans tissues and examined the survival of these animals following Salmonella infection. Here we show that inhibition of the bec-1 gene in the intestine but not in other tissues confers susceptibility to Salmonella infection, which is consistent with recent studies in mice showing that autophagy is involved in clearance of Salmonella in the intestinal epithelial cells. Therefore, the intestinal autophagy activity is essential for host defense against Salmonella infection from C. elegans to mice, perhaps also in humans.
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Date Issued: 2014
PURL: http://purl.flvc.org/fau/fd/FAUIR000527
Format: Document (PDF)

Title: daf-31 Encodes the Catalytic Subunit of N Alpha-Acetyltransferase that Regulates Caenorhabditis elegans Development, Metabolism and Adult Lifespan.
Creator: Chen, Di, Zhang, Jiuli, Minnerly, Justin, Kaul, Tiffany, Riddle, Donald L., Jia, Kailiang, Kim, Stuart K.
Date Issued: 2014-10-16
PURL: http://purl.flvc.org/fau/fd/FAUIR000115
Format: Citation

Title: Intestinal autophagy activity protects against Salmonella typhimurium infection in Caenorhabditis elegans.
Creator: Curt, Alexander L., Jia, Kailiang, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Autophagy is a lysosomal degradation pathway present in eukaryotes that allows a cell to break down cytoplasmic proteins and organelles to maintain homeostasis. The autophagy pathway has been shown to play a significant role in the immune systems protective response against various bacterial pathogen infections, such as the intestinal pathogen Salmonella typhimurium, in Caenorhabditis elegans and in mammals. This study investigated if the autophagy pathway acts in a tissue-specific manner to...
Show moreAutophagy is a lysosomal degradation pathway present in eukaryotes that allows a cell to break down cytoplasmic proteins and organelles to maintain homeostasis. The autophagy pathway has been shown to play a significant role in the immune systems protective response against various bacterial pathogen infections, such as the intestinal pathogen Salmonella typhimurium, in Caenorhabditis elegans and in mammals. This study investigated if the autophagy pathway acts in a tissue-specific manner to protect against S. typhimurium infection in C. elegans. Wild type C. elegans and worms where the autophagy gene bec-1 was inhibited in different tissues by RNAi treatment were infected by S. typhimurium and their survival measured. My data showed that the autophagy gene bec-1 only protected C. elegans against S. typhimurium infection in the intestinal tissues, suggesting that the autophagy pathway acts in a tissue specific manner to help protect against Salmonella invasions in C. elegans.
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Date Issued: 2012
PURL: http://purl.flvc.org/fau/fd/FA00004244
Format: Document (PDF)

Title: Autophagy gene atg-18 regulates C. elegans lifespan cell nonautonomously by neuropeptide signaling.
Creator: Minnerly, Justin, Jia, Kailiang, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: In the round worm C. elegans, it has recently been shown that autophagy, a highly conserved lysosomal degradation pathway that is present in all eukaryotic cells, is required for maintaining healthspan and for increasing the adult lifespan of worms fed under dietary restriction conditions or with reduced IGF signaling. It is currently unknown how extracellular signals regulate autophagy activity within different tissues during these processes and whether autophagy functions cell-autonomously...
Show moreIn the round worm C. elegans, it has recently been shown that autophagy, a highly conserved lysosomal degradation pathway that is present in all eukaryotic cells, is required for maintaining healthspan and for increasing the adult lifespan of worms fed under dietary restriction conditions or with reduced IGF signaling. It is currently unknown how extracellular signals regulate autophagy activity within different tissues during these processes and whether autophagy functions cell-autonomously or nonautonomously. We have data that for the first time shows autophagy activity in the neurons and intestinal cells plays a major role in regulating adult lifespan and the longevity conferred by altered IGF signaling and dietary restriction, suggesting autophagy can control these phenotypes cell non-autonomously. We hypothesize that autophagy in the neurons and intestinal cells is an essential cellular process regulated by different signaling pathways to control wild type adult lifespan, IGF mediated longevity and dietary restriction induced longevity. Excitingly we also have found that in animals with reduced IGF signaling autophagy can control longevity in only a small subset of neurons alone. Autophagy in either specific individual chemosensory neurons or a small group of them is completely sufficient to control IGF mediated longevity. This work provides novel insight to the function and regulation of autophagy which will help shed light on understanding this essential process in higher organisms, including mammals.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00004862, http://purl.flvc.org/fau/fd/FA00004862
Subject Headings: Caenorhabditis elegans--Molecular genetics., Aging--Molecular aspects., Life cycles (Biology), Cell death., Gene expression., Autophagic vacuoles., Apoptosis., Eukaryotic cells.
Format: Document (PDF)

Title: Analysis of the Role of Autophagy in Dauer Formation and Dauer Recovery Regulated by TGF-β Signaling Pathway in Caenorhabditis elegans.
Creator: Ritter, Portia, Jia, Kailiang, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Caenorhabditis elegans optionally enter into a dauer diapause phase that results in a prolonged life in a semi-dormant state. Entry into and recovery from dauer diapause includes many physical changes in body structure, physiology, and gene expression. Entry into dauer diapause is regulated by several signaling pathways including transforming growth factor (TGF-β). Autophagy plays an important role in dauer formation and recover. During dauer transformation autophagy is up-regulated and may...
Show moreCaenorhabditis elegans optionally enter into a dauer diapause phase that results in a prolonged life in a semi-dormant state. Entry into and recovery from dauer diapause includes many physical changes in body structure, physiology, and gene expression. Entry into dauer diapause is regulated by several signaling pathways including transforming growth factor (TGF-β). Autophagy plays an important role in dauer formation and recover. During dauer transformation autophagy is up-regulated and may play a role in remodeling the molecular structure for long term survival during dauer diapause. This research helps determine the role of autophagy in dauer development and recovery mediated through the TGF-β signaling pathway. This research also determines in which tissue autophagy is necessary for dauer formation and recovery through TGF-β signaling. This research is shedding light on the function of autophagy in the TGF-β signaling pathway, both processes of which have been linked to tumorigenesis, heart disease and cancer.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00004921, http://purl.flvc.org/fau/fd/FA00004921
Subject Headings: Aging--Molecular aspects., Aging--Physiological aspects., Caenorhabditis elegans--Molecular genetics., Autophagic vacuoles., Gene expression., Apoptosis., Cellular signal transduction., DNA-binding proteins., Transforming growth factors-beta--Receptors.
Format: Document (PDF)

Title: A neuronal G protein-coupled receptor mediates the effect of diet on lifespan and development in Caenorhabditis elegans through autophagy.
Creator: Parker, Thomas A., Jia, Kailiang, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Animals rely on the integration of a variety of external cues to understand and respond appropriately to their environment. The relative amounts of food and constitutively secreted pheromone detected by the nematode C. elegans determines how it will develop and grow. Starvation conditions cause the animal to enter a protective stage, termed dauer. Dauer animals are non-eating, long-lived and stress resistant. Yet, when these animals are introduced to food replete conditions they will recover...
Show moreAnimals rely on the integration of a variety of external cues to understand and respond appropriately to their environment. The relative amounts of food and constitutively secreted pheromone detected by the nematode C. elegans determines how it will develop and grow. Starvation conditions cause the animal to enter a protective stage, termed dauer. Dauer animals are non-eating, long-lived and stress resistant. Yet, when these animals are introduced to food replete conditions they will recover from dauer and proceed into normal development. Furthermore, food restriction has been demonstrated to extend the lifespan of a wide-range of species including C. elegans. However, the exact mechanism by which food signals are detected and transduced by C. elegans to influence development and longevity remains unknown. Here, we identify a G protein-coupled receptor (GPCR) DCAR-1 that acts in two chemosensory neurons to mediate food signaling in an autophagy-related manner. The DCAR-1 ligand Dihydrocaffeic acid (DHCA) competes with dauer-inducing pheromone to promote growth. DHCA is a key intermediate in the shikimate pathway, which is required to synthesize folate and aromatic amino acids. We report that dcar-1 mutations influence dauer formation and extend wildtype lifespan via a mechanism of dietary restriction. Moreover, we show that the lifespan extension of dcar-1 mutants is completely dependent on autophagy gene atg- 18. Furthermore, our data suggests metabolites derived from shikimate are food signals that control aging and dauer development through GPCR signaling in C. elegans. These studies will contribute to the delineation of mechanisms behind the beneficial effects of dietary restriction in eukaryotic organisms.
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Date Issued: 2019
PURL: http://purl.flvc.org/fau/fd/FA00013338
Subject Headings: Caenorhabditis elegans, Autophagy, Receptors, G-Protein-Coupled, Longevity, Diet
Format: Document (PDF)

Title: Aberrant Autolysosomal Regulation Is Linked to The Induction of Embryonic Senescence: Differential Roles of Beclin 1 and p53 in Vertebrate Spns1 Deficien.
Creator: Tomoyuki Sasaki, Shanshan Lian, Jie Qi, Peter E. Bayliss, Christopher E. Carr, Jennifer L. Johnson, Sujay Guha, Patrick Kobler, Sergio D. Catz, Matthew Gill, Kailiang Jia, Daniel J. Klionsky
Abstract/Description: Spinster (Spin) in Drosophila or Spinster homolog 1 (Spns1) in vertebrates is a putative lysosomal H+-carbohydrate transporter, which functions at a late stage of autophagy. The Spin/Spns1 defect induces aberrant autolysosome formation that leads to embryonic senescence and accelerated aging symptoms, but little is known about the mechanisms leading to the pathogenesis in vivo. Beclin 1 and p53 are two pivotal tumor suppressors that are critically involved in the autophagic process and its...
Show moreSpinster (Spin) in Drosophila or Spinster homolog 1 (Spns1) in vertebrates is a putative lysosomal H+-carbohydrate transporter, which functions at a late stage of autophagy. The Spin/Spns1 defect induces aberrant autolysosome formation that leads to embryonic senescence and accelerated aging symptoms, but little is known about the mechanisms leading to the pathogenesis in vivo. Beclin 1 and p53 are two pivotal tumor suppressors that are critically involved in the autophagic process and its regulation. Using zebrafish as a genetic model, we show that Beclin 1 suppression ameliorates Spns1 lossmediated senescence as well as autophagic impairment, whereas unexpectedly p53 deficit exacerbates both of these characteristics. We demonstrate that ‘basal p53’ activity plays a certain protective role(s) against the Spns1 defect-induced senescence via suppressing autophagy, lysosomal biogenesis, and subsequent autolysosomal formation and maturation, and that p53 loss can counteract the effect of Beclin 1 suppression to rescue the Spns1 defect. By contrast, in response to DNA damage, ‘activated p53’ showed an apparent enhancement of the Spns1-deficient phenotype, by inducing both autophagy and apoptosis. Moreover, we found that a chemical and genetic blockage of lysosomal acidification and biogenesis mediated by the vacuolar-type H+-ATPase, as well as of subsequent autophagosome-lysosome fusion, prevents the appearance of the hallmarks caused by the Spns1 deficiency, irrespective of the basal p53 state. Thus, these results provide evidence that Spns1 operates during autophagy and senescence differentially with Beclin 1 and p53.
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Date Issued: 2014
PURL: http://purl.flvc.org/fau/fd/FAUIR000526
Format: Document (PDF)

Title: Modulating Behavior in C. elegans Using Electroshock and Antiepileptic Drugs.
Creator: Monica G. Risley, Stephanie P. Kelly, Kailiang Jia, Brock Grill, Ken Dawson- Scully
Abstract/Description: The microscopic nematode Caenorhabditis elegans has emerged as a valuable model for understanding the molecular and cellular basis of neurological disorders. The worm offers important physiological similarities to mammalian models such as conserved neuron morphology, ion channels, and neurotransmitters. While a wide-array of behavioral assays are available in C. elegans, an assay for electroshock/electroconvulsion remains absent. Here, we have developed a quantitative behavioral method to...
Show moreThe microscopic nematode Caenorhabditis elegans has emerged as a valuable model for understanding the molecular and cellular basis of neurological disorders. The worm offers important physiological similarities to mammalian models such as conserved neuron morphology, ion channels, and neurotransmitters. While a wide-array of behavioral assays are available in C. elegans, an assay for electroshock/electroconvulsion remains absent. Here, we have developed a quantitative behavioral method to assess the locomotor response following electric shock in C. elegans. Electric shock impairs normal locomotion, and induces paralysis and muscle twitching; after a brief recovery period, shocked animals resume normal locomotion. We tested electric shock responses in loss-of-function mutants for unc-25, which encodes the GABA biosynthetic enzyme GAD, and unc-49, which encodes the GABAA receptor. unc-25 and unc-49 mutants have decreased inhibitory GABAergic transmission to muscles, and take significantly more time to recover normal locomotion following electric shock compared to wild-type. Importantly, increased sensitivity of unc-25 and unc-49 mutants to electric shock is rescued by treatment with antiepileptic drugs, such as retigabine. Additionally, we show that pentylenetetrazol (PTZ), a GABAA receptor antagonist and proconvulsant in mammalian and C. elegans seizure models, increases susceptibility of worms to electric shock.
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FAUIR000530
Format: Document (PDF)

Title: egl‑4 modulates electroconvulsive seizure duration in C. elegans.
Creator: Monica G. Risley, Stephanie P. Kelly, Justin Minnerly, Kailiang Jia, Ken Dawson‑Scully
Abstract/Description: Increased neuronal excitability causes seizures with debilitating symptoms. Effective and noninvasive treatments are limited for easing symptoms, partially due to the complexity of the disorder and lack of knowledge of specific molecular faults. An unexplored, novel target for seizure therapeutics is the cGMP/protein kinase G (PKG) pathway, which targets downstream K+ channels, a mechanism similar to Retigabine, a recently FDA-approved antiepileptic drug. Our results demonstrate that...
Show moreIncreased neuronal excitability causes seizures with debilitating symptoms. Effective and noninvasive treatments are limited for easing symptoms, partially due to the complexity of the disorder and lack of knowledge of specific molecular faults. An unexplored, novel target for seizure therapeutics is the cGMP/protein kinase G (PKG) pathway, which targets downstream K+ channels, a mechanism similar to Retigabine, a recently FDA-approved antiepileptic drug. Our results demonstrate that increased PKG activity decreased seizure duration in C. elegans utilizing a recently developed electroconvulsive seizure assay. While the fly is a well-established seizure model, C. elegans are an ideal yet unexploited model which easily uptakes drugs and can be utilized for high-throughput screens. In this study, we show that treating the worms with either a potassium channel opener, Retigabine or published pharmaceuticals that increase PKG activity, significantly reduces seizure recovery times. Our results suggest that PKG signaling modulates downstream K+ channel conductance to control seizure recovery time in C. elegans. Hence, we provide powerful evidence, suggesting that pharmacological manipulation of the PKG signaling cascade may control seizure duration across phyla.
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Date Issued: 2018
PURL: http://purl.flvc.org/fau/fd/FAUIR000532
Format: Document (PDF)

Title: Guidelines for monitoring autophagy in Caenorhabditis elegans.
Creator: Hong Zhang, Jessica T Chang, Bin Guo, Malene Hansen, Kailiang Jia, Attila L Kovács, Caroline Kumsta, Louis R Lapierre, Renaud Legouis, Long Lin, Qun Lu, Alicia Meléndez, Eyleen J O'Rourke, Ken Sato, Miyuki Sato, Xiaochen Wang, Fan Wu
Abstract/Description: The cellular recycling process of autophagy has been extensively characterized with standard assays in yeast and mammalian cell lines. In multicellular organisms, numerous external and internal factors differentially affect autophagy activity in specific cell types throughout the stages of organismal ontogeny, adding complexity to the analysis of autophagy in these metazoans. Here we summarize currently available assays for monitoring the autophagic process in the nematode C. elegans. A...
Show moreThe cellular recycling process of autophagy has been extensively characterized with standard assays in yeast and mammalian cell lines. In multicellular organisms, numerous external and internal factors differentially affect autophagy activity in specific cell types throughout the stages of organismal ontogeny, adding complexity to the analysis of autophagy in these metazoans. Here we summarize currently available assays for monitoring the autophagic process in the nematode C. elegans. A combination of measuring levels of the lipidated Atg8 ortholog LGG-1, degradation of well characterized autophagic substrates such as germline P granule components and the SQSTM1/p62 ortholog SQST-1, expression of autophagic genes and electron microscopy analysis of autophagic structures are presently the most informative, yet steady-state, approaches available to assess autophagy levels in C. elegans. We also review how altered autophagy activity affects a variety of biological processes in C. elegans such as L1 survival under starvation conditions, dauer formation, aging, and cell death, as well as neuronal cell specification. Taken together, C. elegans is emerging as a powerful model organism to monitor autophagy while evaluating important physiological roles for autophagy in key developmental events as well as during adulthood.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FAUIR000529
Format: Document (PDF)

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