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Neuronal autophagy activity is essential for insulin growth factor signaling-regulated lifespan extension in C. elegans
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)
Tissue-specific requirement of the autophagy gene atg-18 in controlling C. elegans dauer morphogenesis, fat metabolism and adult longevity
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)
A Protocol to Infect Caenorhabditis elegans with Salmonella typhimuri
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)
The cell non-autonomous function of ATG-18 is essential for neuroendocrine regulation of Caenorhabditis elegans lifespan
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)
Intestinal autophagy activity is essential for host defense against Salmonella typhimurium infection in Caenorhabditis elega
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)
daf-31 Encodes the Catalytic Subunit of N Alpha-Acetyltransferase that Regulates Caenorhabditis elegans Development, Metabolism and Adult Lifespan
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