Alternate metabolism during the dauer stage of the nematode Caenorhabditis elegans

Burnell, Ann M.; Houthoofd, Koen; O’Hanlon, Karen; Vanfleteren, Jacques R.

doi:10.1016/j.exger.2005.09.006

Cited by 143 publications

(161 citation statements)

References 36 publications

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“…Data are presented as the mean from two to four independent experiments 6 SEM. protein turnover rates in dauer animals (Burnell et al 2005;Jones et al 2010). Interestingly, although glucose stress resulted in a slight increase in O-GlcNAcylation in the daf-2;oga-1 background, the magnitude was much less than that observed in the wild-type background (compare Figure 1F to Figure 3B), which may suggest an altered steady state in the absence of insulin signaling.…”

Section: Resultsmentioning

confidence: 70%

O-Linked-N-Acetylglucosamine Cycling and Insulin Signaling Are Required for the Glucose Stress Response inCaenorhabditis elegans

et al. 2011

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In a variety of organisms, including worms, flies, and mammals, glucose homeostasis is maintained by insulin-like signaling in a robust network of opposing and complementary signaling pathways. The hexosamine signaling pathway, terminating in O-linked-N-acetylglucosamine (O-GlcNAc) cycling, is a key sensor of nutrient status and has been genetically linked to the regulation of insulin signaling in Caenorhabditis elegans. Here we demonstrate that O-GlcNAc cycling and insulin signaling are both essential components of the C. elegans response to glucose stress. A number of insulin-dependent processes were found to be sensitive to glucose stress, including fertility, reproductive timing, and dauer formation, yet each of these differed in their threshold of sensitivity to glucose excess. Our findings suggest that O-GlcNAc cycling and insulin signaling are both required for a robust and adaptable response to glucose stress, but these two pathways show complex and interdependent roles in the maintenance of glucose-insulin homeostasis.

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Section: Resultsmentioning

confidence: 70%

O-Linked-N-Acetylglucosamine Cycling and Insulin Signaling Are Required for the Glucose Stress Response inCaenorhabditis elegans

et al. 2011

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“…During dauer formation, NADPH, a major reducing agent, is required for the production of fatty acids and depository triglycerides 4,39 . A shutdown of the PPP at the organismal level would thus be deleterious for the long-term survival of the dauers.…”

Section: Discussionmentioning

confidence: 99%

Integration of carbohydrate metabolism and redox state controls dauer larva formation in Caenorhabditis elegans

et al. 2015

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Under adverse conditions, Caenorhabditis elegans enters a diapause stage called the dauer larva. External cues signal the nuclear hormone receptor DAF-12, the activity of which is regulated by its ligands: dafachronic acids (DAs). DAs are synthesized from cholesterol, with the last synthesis step requiring NADPH, and their absence stimulates dauer formation. Here we show that NADPH levels determine dauer formation in a regulatory mechanism involving key carbohydrate and redox metabolic enzymes. Elevated trehalose biosynthesis diverts glucose-6-phosphate from the pentose phosphate pathway, which is the major source of cellular NADPH. This enhances dauer formation due to the decrease in the DA level. Moreover, DAF-12, in cooperation with DAF-16/FoxO, induces negative feedback of DA synthesis via activation of the trehalose-producing enzymes TPS-1/2 and inhibition of the NADPH-producing enzyme IDH-1. Thus, the dauer developmental decision is controlled by integration of the metabolic flux of carbohydrates and cellular redox potential.

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“…In the daf-2(e1370) animal, which has a mutation in the insulin receptor kinase domain, the DAF-16 protein is translocated to the nucleus. Phenotypes observed in the daf-2(e1370) animal include constitutive dauer formation at increased temperature, alteration in gene expression, increased longevity, resistance to a variety of stresses, and changes in metabolism (Kenyon et al 1993;Vanfleteren and De Vreese 1996;Kimura et al 1997;Ogg et al 1997;Gems et al 1998;Lee et al 2003;McElwee et al 2003McElwee et al , 2004Munoz 2003;Murphy et al 2003;Van Voorhies 2003;Burnell et al 2005). DNA microarray studies determined that genes involved with stress response and metabolism are upregulated in the daf-2 mutant.…”

mentioning

confidence: 99%

Glyceraldehyde-3-Phosphate Dehydrogenase Mediates Anoxia Response and Survival in Caenorhabditis elegans

2006

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Oxygen deprivation has a role in the pathology of many human diseases. Thus it is of interest in understanding the genetic and cellular responses to hypoxia or anoxia in oxygen-deprivation-tolerant organisms such as Caenorhabditis elegans. In C. elegans the DAF-2/DAF-16 pathway, an IGF-1/insulin-like signaling pathway, is involved with dauer formation, longevity, and stress resistance. In this report we compared the response of wild-type and daf-2(e1370) animals to anoxia. Unlike wild-type animals, the daf-2(e1370) animals have an enhanced anoxia-survival phenotype in that they survive long-term anoxia and hightemperature anoxia, do not accumulate significant tissue damage in either of these conditions, and are motile after 24 hr of anoxia. RNA interference was used to screen DAF-16-regulated genes that suppress the daf-2(e1370)-enhanced anoxia-survival phenotype. We identified gpd-2 and gpd-3, two nearly identical genes in an operon that encode the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase. We found that not only is the daf-2(e1370)-enhanced anoxia phenotype dependent upon gpd-2 and gpd-3, but also the motility of animals exposed to brief periods of anoxia is prematurely arrested in gpd-2/3(RNAi) and daf-2(e1370);gpd-2/3(RNAi) animals. These data suggest that gpd-2 and gpd-3 may serve a protective role in tissue exposed to oxygen deprivation.

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Alternate metabolism during the dauer stage of the nematode Caenorhabditis elegans

Cited by 143 publications

References 36 publications

O-Linked-N-Acetylglucosamine Cycling and Insulin Signaling Are Required for the Glucose Stress Response inCaenorhabditis elegans

O-Linked-N-Acetylglucosamine Cycling and Insulin Signaling Are Required for the Glucose Stress Response inCaenorhabditis elegans

Integration of carbohydrate metabolism and redox state controls dauer larva formation in Caenorhabditis elegans

Glyceraldehyde-3-Phosphate Dehydrogenase Mediates Anoxia Response and Survival in Caenorhabditis elegans

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