Detection of Autophagy in <i>Caenorhabditis elegans</i> Using <i>GFP::LGG-1</i> as an Autophagy Marker

Palmisano, Nicholas J.; Meléndez, Alicia

doi:10.1101/pdb.prot086496

Cited by 22 publications

(29 citation statements)

References 118 publications

(257 reference statements)

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“…Autophagy was assessed using the QU1 izEx1[Plgg-1::gfp::lgg-1+rol-6] (LGG-1::GFP) reporter strain, where increased or impaired autophagic flux is represented by a change in the number ofLGG-1::GFP foci (Palmisano and Melendez 2016b), using the experimental design for Experiment 1. Nematodes were reared to the young adult stage and exposed to control conditions, HgCl 2 (1 and 5 μM), or MeHgCl (1 and 5 μM) for 24hr.…”

Section: Methodsmentioning

confidence: 99%

Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans

et al. 2017

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Mercury toxicity mechanisms have the potential to induce DNA damage and disrupt cellular processes, like mitochondrial function. Proper mitochondrial function is important for cellular bioenergetics and immune signaling and function. Impacts of mercury on the nuclear genome (nDNA) are conflicting and inconclusive, and mitochondrial DNA (mtDNA) impacts are relatively unknown. In this study, we assessed genotoxic (mtDNA and nDNA), metabolic, and innate immune impacts of inorganic and organic mercury exposure in Caenorhabditis elegans. Genotoxic outcomes measured included DNA damage, DNA damage repair (nucleotide excision repair, NER; base excision repair, BER), and genomic copy number following MeHg and HgCl2 exposure alone and in combination with known DNA damage-inducing agents ultraviolet C radiation (UVC) and hydrogen peroxide (H2O2), which cause bulky DNA lesions and oxidative DNA damage, respectively. Following exposure to both MeHg and HgCl2, low-level DNA damage (~0.25 lesions/10 kb mtDNA and nDNA) was observed. Unexpectedly, a higher MeHg concentration reduced damage in both genomes compared to controls. However, this observation was likely the result of developmental delay. In co-exposure treatments, both mercury compounds increased initial DNA damage (mtDNA and nDNA) in combination with H2O2 exposure, but had no impact in combination with UVC exposure. Mercury exposure both increased and decreased DNA damage removal via BER. DNA repair after H2O2 exposure in mercury-exposed nematodes resulted in damage levels lower than measured in controls. Impacts to NER were not detected. mtDNA copy number was significantly decreased in the MeHg-UVC and MeHg-H2O2 co-exposure treatments. Mercury exposure had metabolic impacts (steady-state ATP levels) that differed between the compounds; HgCl2 exposure decreased these levels, while MeHg slightly increased levels or had no impact. Both mercury species reduced mRNA levels for immune signaling-related genes, but had mild or no effects on survival on pathogenic bacteria. Overall, mercury exposure disrupted mitochondrial endpoints in a mercury-compound dependent fashion.

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Section: Methodsmentioning

confidence: 99%

Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans

et al. 2017

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“…Similar methods to study autophagy have been used in invertebrate model organisms and mammalian systems with the employment of the benefits of every system. These methods are recently reviewed in detail for yeast [17][18][19][20], C. elegans [21][22][23][24][25], flies [26][27][28][29][30], and mammalian systems [31][32][33][34][35][36].…”

Section: Methods To Monitor Autophagy In Model Organismsmentioning

confidence: 99%

Autophagy in Model Organisms: Insights into Cancer

Possik¹,

Pause²

2016

Autophagy in Current Trends in Cellular Physiology and Pathology

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Autophagy is an evolutionarily conserved process utilized by most organisms to clear cellular damage and recycle building blocks for energy production. In this chapter, we emphasize the importance of genetic model organisms, including yeast, nematodes, flies, and mammals in the discovery and understanding of the autophagy process. We highlight the important roles of autophagy in aging, stress tolerance, neuronal health, organismal development, and pathogen resistance in invertebrate and vertebrate model organisms. We provide examples on how the same autophagy-related pathways that increase stress response and longevity in lower organisms could be utilized by cancer cells to survive harsh microenvironments, proliferate, and metastasize, with emphasis on the dual role of autophagy in cancer: an antitumorigenic or a protumorigenic process.

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“…LGG-1+rol-6 (su1006)] IR2686: acbp-1(sv62)I; daf-2(e1370)III. Autophagy was measured as described in the literature 38 . For measuring LGG-1/LC-3 puncta, 10 well-fed adult worms of the respective genetic backgrounds were allowed to lay eggs on nematode growth medium or RNAi plates.…”

Section: Elegans Experimentsmentioning

confidence: 99%

Acyl-CoA-binding protein (ACBP): a phylogenetically conserved appetite stimulator

et al. 2020

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Recently, we reported that, in mice, hunger causes the autophagy-dependent release of a protein called "acyl-CoAbinding protein" or "diazepam binding inhibitor" (ACBP/DBI) from cells, resulting in an increase in plasma ACBP concentrations. Administration of extra ACBP is orexigenic and obesogenic, while its neutralization is anorexigenic in mice, suggesting that ACBP is a major stimulator of appetite and lipo-anabolism. Accordingly, obese persons have higher circulating ACBP levels than lean individuals, and anorexia nervosa is associated with subnormal ACBP plasma concentrations. Here, we investigated whether ACBP might play a phylogenetically conserved role in appetite stimulation. We found that extracellular ACBP favors sporulation in Saccharomyces cerevisiae, knowing that sporulation is a strategy for yeast to seek new food sources. Moreover, in the nematode Caenorhabditis elegans, ACBP increased the ingestion of bacteria as well as the frequency pharyngeal pumping. These observations indicate that ACBP has a phylogenetically ancient role as a 'hunger factor' that favors food intake. Recently, we identified acyl-CoA-binding protein (ACBP), also known as diazepam binding inhibitor (DBI), as a novel appetite stimulating factor 19. Indeed, plasma concentrations of ACBP are elevated in obese patients, as well as in mice that were rendered obese by a high-fat diet

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Detection of Autophagy in Caenorhabditis elegans Using GFP::LGG-1 as an Autophagy Marker

Cited by 22 publications

References 118 publications

Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans

Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans

Autophagy in Model Organisms: Insights into Cancer

Acyl-CoA-binding protein (ACBP): a phylogenetically conserved appetite stimulator

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