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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)
The Role of Mitophagy in the Longevity of Caenorhabditis elegans
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)
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)
Identification of C. elegans ortholog of spinster
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)
A Caenorhabditis elegans Model of Age-dependent Neurodegeneration
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)