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21 results on '"Olivares, Gonzalo H."'

6. Early-life nutrition interacts with developmental genes to shape the brain and sleep behavior in Drosophila melanogaster

Author

Olivares, Gonzalo H, primary, Núñez-Villegas, Franco, additional, Candia, Noemi, additional, Oróstica, Karen, additional, González-Ramírez, M Constanza, additional, Vega-Macaya, Franco, additional, Zúñiga, Nolberto, additional, Molina, Cristian, additional, Oliva, Carlos, additional, Mackay, Trudy F C, additional, Verdugo, Ricardo A, additional, and Olguín, Patricio, additional

Published
2023
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7. Supp_Figs_caption from Low-nutrient diet in Drosophila larvae stage causes enhancement in dopamine modulation in adult brain due epigenetic imprinting

Author

Zúñiga-Hernández, J. M., Olivares, Gonzalo H., Olguín, Patricio, and Glavic, Alvaro

Abstract

Nutrient scarcity is a frequent adverse condition that organisms face during their development. This condition may lead to long-lasting effects on the metabolism and behaviour of adults due to developmental epigenetic modifications. Here, we show that reducing nutrient availability during larval development affects adult spontaneous activity and sleep behaviour, together with changes in gene expression and epigenetic marks in the Mushroom bodies (MBs). We found that open chromatin regions map to 100 of 241 transcriptionally upregulated genes in the adult MBs, these new opening zones are preferentially located in regulatory zones such as promoter-TSS and introns. Importantly, opened chromatin at the Dopamine 1-like receptor 2 transcription start site correlates with increased expression. Thus, adult administration of a dopamine antagonist reverses increased spontaneous activity and diminished sleep time observed in response to early-life nutrient restriction. In comparison, reducing dop1R2 expression in MBs also ameliorates these effects, albeit to a lesser degree. These results lead to the conclusion that increased dopamine signalling in the MBs of flies reared in a poor nutritional environment underlies the behavioural changes observed due to this condition during development.

Published
2023
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9. Syndecan-1 regulates BMP signaling and dorso-ventral patterning of the ectoderm during early Xenopus development

Author

Olivares, Gonzalo H., Carrasco, HeCtor, Aroca, Francisco, Carvallo, Loreto, Segovia, FabiaN, and Larrain, Juan

Subjects
Embryonic development, Sulfates, Messenger RNA, Proteoglycans, Growth factors, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.03.007 Byline: Gonzalo H. Olivares, Hector Carrasco, Francisco Aroca, Loreto Carvallo, Fabian Segovia, Juan Larrain Keywords: Syndecan1; HSPG; BMP signaling; Dorso-ventral patterning; Ectoderm; Chordin Abstract: Extracellular regulation of growth factor signaling is a key event for embryonic patterning. Heparan sulfate proteoglycans (HSPG) are among the molecules that regulate this signaling during embryonic development. Here we study the function of syndecan1 (Syn1), a cell-surface HSPG expressed in the non-neural ectoderm during early development of Xenopus embryos. Overexpression of Xenopus Syn1 (xSyn1) mRNA is sufficient to reduce BMP signaling, induce chordin expression and rescue dorso-ventral patterning in ventralized embryos. Experiments using chordin morpholinos established that xSyn1 mRNA can inhibit BMP signaling in the absence of chordin. Knockdown of xSyn1 resulted in a reduction of BMP signaling and expansion of the neural plate with the concomitant reduction of the non-neural ectoderm. Overexpression of xSyn1 mRNA in xSyn1 morphant embryos resulted in a biphasic effect, with BMP being inhibited at high concentrations and activated at low concentrations of xSyn1. Interestingly, the function of xSyn1 on dorso-ventral patterning and BMP signaling is specific for this HSPG. In summary, we report that xSyn1 regulates dorso-ventral patterning of the ectoderm through modulation of BMP signaling. Author Affiliation: Center for Aging and Regeneration, Center for Cell Regulation and Pathology, MIFAB, Faculty of Biological Sciences, P. Universidad Catolica de Chile, Alameda 340, Santiago, Chile Article History: Received 1 September 2008; Revised 6 March 2009; Accepted 6 March 2009

Published
2009

17. Expression of Transposable Elements in Neural Tissues during Xenopus Development

Author

Faunes, Fernando, primary, Sanchez, Natalia, additional, Moreno, Mauricio, additional, Olivares, Gonzalo H., additional, Lee-Liu, Dasfne, additional, Almonacid, Leonardo, additional, Slater, Alex W., additional, Norambuena, Tomas, additional, Taft, Ryan J., additional, Mattick, John S., additional, Melo, Francisco, additional, and Larrain, Juan, additional

Published
2011
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21. Wnt-3a overcomes beta-amyloid toxicity in rat hippocampal neurons.

Author

Alvarez AR, Godoy JA, Mullendorff K, Olivares GH, Bronfman M, and Inestrosa NC

Subjects
Alzheimer Disease genetics, Alzheimer Disease metabolism, Alzheimer Disease physiopathology, Amyloid beta-Peptides metabolism, Amyloid beta-Peptides toxicity, Animals, Apoptosis drug effects, Apoptosis physiology, Cell Survival drug effects, Cell Survival physiology, Cells, Cultured, Culture Media, Conditioned pharmacology, Cytoskeletal Proteins drug effects, Cytoskeletal Proteins metabolism, Glycogen Synthase Kinase 3 drug effects, Glycogen Synthase Kinase 3 metabolism, Glycogen Synthase Kinase 3 beta, Hippocampus cytology, Hippocampus embryology, Homeodomain Proteins drug effects, Homeodomain Proteins metabolism, Ligands, Nerve Degeneration drug therapy, Nerve Degeneration prevention & control, Nerve Tissue Proteins drug effects, Nerve Tissue Proteins metabolism, Neurons drug effects, Neurons pathology, Neuroprotective Agents pharmacology, Oxidative Stress drug effects, Oxidative Stress physiology, Phosphorylation drug effects, Proteins agonists, Proteins pharmacology, Rats, Rats, Sprague-Dawley, Signal Transduction drug effects, Signal Transduction physiology, Trans-Activators drug effects, Trans-Activators metabolism, Up-Regulation drug effects, Up-Regulation physiology, Wnt Proteins, Wnt3 Protein, beta Catenin, tau Proteins drug effects, tau Proteins metabolism, Amyloid beta-Peptides antagonists & inhibitors, Nerve Degeneration metabolism, Neurons metabolism, Neuroprotective Agents metabolism, Proteins metabolism
Abstract

The aim of this study was to evaluate whether the direct activation of the Wnt signaling pathway by its endogenous Wnt-3a ligand prevents the toxic effects induced by amyloid-beta-peptide (Abeta) in rat hippocampal neurons. We report herein that the Wnt-3a ligand was indeed able to overcome toxic effects induced by Abeta in hippocampal neurons, including a neuronal impairment on cell survival, an increase in glycogen synthase kinase-3beta (GSK-3beta) and tau phosphorylation, a decrease in cytoplasmic beta-catenin and a decrease in the expression of the Wnt target gene engrailed-1. We further demonstrate that Wnt-3a protects hippocampal neurons from apoptosis induced by Abeta. Our results support the hypothesis that a loss of function of Wnt signaling may play a role in the progression of neurodegenerative diseases such as Alzheimer's disease.

Published
2004
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