scholarly journals Zebrafish Embryo as an Emerging Model Organism in Neurodevelopmental Toxicity Research

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Şükriye Çalışkan ◽  
Ebru Emekli Alturfan
2001 ◽  
Vol 360 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Takeshi YABU ◽  
Shuji KISHI ◽  
Toshiro OKAZAKI ◽  
Michiaki YAMASHITA

Caspase-3 was cloned from zebrafish embryos and its properties were characterized to identify the biological implications of caspase in embryogenesis and apoptosis in zebrafish, which is a model organism in vertebrate developmental biology and genetics. The predicted amino acid sequence, totalling 282 amino acid residues, consisted of the prodomain and large and small subunits. Phylogenetic analysis showed that the cloned zebrafish caspase was a member of the caspase-3 subfamily with approx. 60% identity with caspase-3 from Xenopus, chicken and mammals. In addition, recombinant zebrafish caspase hydrolysed acetyl-Asp-Glu-Val-Asp-4-methyl-coumaryl-7-amide, and exhibited similar substrate specificity to the mammalian caspase-3 subfamily. Therefore this caspase was designated zebrafish caspase-3. Overexpression of zebrafish caspase-3 induced apoptosis and increased ceramide levels in fish fathead minnow tailbud cells and zebrafish embryos. Both ceramide generation and apoptosis induction were inhibited by treatment with a caspase inhibitor, benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone. Moreover, zebrafish caspase-3 mRNA was present in early embryos up to the 1000-cell stage as a maternal factor, and was then expressed throughout the body after the gastrula stage by zygotic expression. These findings indicate that the isolated caspase-3 plays an important role in the induction of ceramide generation as well as apoptosis in fish cells and the zebrafish embryo, and suggest that caspase-3 functions as a modulator of the pro-apoptotic signal in development.


2017 ◽  
Author(s):  
Rabea Bluemel ◽  
Eva Klopocki ◽  
Daniel Liedtke
Keyword(s):  

2020 ◽  
Author(s):  
CC Kim ◽  
GR Healey ◽  
WJ Kelly ◽  
ML Patchett ◽  
Z Jordens ◽  
...  

© 2019, International Society for Microbial Ecology. Pectin is abundant in modern day diets, as it comprises the middle lamellae and one-third of the dry carbohydrate weight of fruit and vegetable cell walls. Currently there is no specialized model organism for studying pectin fermentation in the human colon, as our collective understanding is informed by versatile glycan-degrading bacteria rather than by specialist pectin degraders. Here we show that the genome of Monoglobus pectinilyticus possesses a highly specialized glycobiome for pectin degradation, unique amongst Firmicutes known to be in the human gut. Its genome encodes a simple set of metabolic pathways relevant to pectin sugar utilization, and its predicted glycobiome comprises an unusual distribution of carbohydrate-active enzymes (CAZymes) with numerous extracellular methyl/acetyl esterases and pectate lyases. We predict the M. pectinilyticus degradative process is facilitated by cell-surface S-layer homology (SLH) domain-containing proteins, which proteomics analysis shows are differentially expressed in response to pectin. Some of these abundant cell surface proteins of M. pectinilyticus share unique modular organizations rarely observed in human gut bacteria, featuring pectin-specific CAZyme domains and the cell wall-anchoring SLH motifs. We observed M. pectinilyticus degrades various pectins, RG-I, and galactan to produce polysaccharide degradation products (PDPs) which are presumably shared with other inhabitants of the human gut microbiome (HGM). This strain occupies a new ecological niche for a primary degrader specialized in foraging a habitually consumed plant glycan, thereby enriching our understanding of the diverse community profile of the HGM.


2019 ◽  
Vol 26 (39) ◽  
pp. 6976-6990 ◽  
Author(s):  
Ana María González-Paramás ◽  
Begoña Ayuda-Durán ◽  
Sofía Martínez ◽  
Susana González-Manzano ◽  
Celestino Santos-Buelga

: Flavonoids are phenolic compounds widely distributed in the human diet. Their intake has been associated with a decreased risk of different diseases such as cancer, immune dysfunction or coronary heart disease. However, the knowledge about the mechanisms behind their in vivo activity is limited and still under discussion. For years, their bioactivity was associated with the direct antioxidant and radical scavenging properties of phenolic compounds, but nowadays this assumption is unlikely to explain their putative health effects, or at least to be the only explanation for them. New hypotheses about possible mechanisms have been postulated, including the influence of the interaction of polyphenols and gut microbiota and also the possibility that flavonoids or their metabolites could modify gene expression or act as potential modulators of intracellular signaling cascades. This paper reviews all these topics, from the classical view as antioxidants in the context of the Oxidative Stress theory to the most recent tendencies related with the modulation of redox signaling pathways, modification of gene expression or interactions with the intestinal microbiota. The use of C. elegans as a model organism for the study of the molecular mechanisms involved in biological activity of flavonoids is also discussed.


F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 683 ◽  
Author(s):  
Terry K. Smith ◽  
Frédéric Bringaud ◽  
Derek P. Nolan ◽  
Luisa M. Figueiredo

Cellular metabolic activity is a highly complex, dynamic, regulated process that is influenced by numerous factors, including extracellular environmental signals, nutrient availability and the physiological and developmental status of the cell. The causative agent of sleeping sickness, Trypanosoma brucei, is an exclusively extracellular protozoan parasite that encounters very different extracellular environments during its life cycle within the mammalian host and tsetse fly insect vector. In order to meet these challenges, there are significant alterations in the major energetic and metabolic pathways of these highly adaptable parasites. This review highlights some of these metabolic changes in this early divergent eukaryotic model organism.


Author(s):  
Cynthia D. Trowbridge

The stenophagous ascoglossan (=sacoglossan) opisthobranch Elysia viridis has long been a model organism for the study of endosymbiosis or kleptoplasty as well as one of the few herbivores to consume the introduced green macroalga Codium fragile on European shores. Larval and post-larval dynamics of the ascoglossan were investigated. Planktotrophic larvae of E. viridis grew at 5–10 μm d−1 (shell length) at 15°C on a unicellular algal diet (the cryptophyte Rhodomonas baltica); larvae became competent one month post-hatching. Effective feeding and chloroplast acquisition typically started within 2–3 d of metamorphosis. Slugs grew about 8 mm in the first month of post-larval life. During this period, juveniles held in the light did not grow faster or survive better than conspecifics held in the dark; thus, functional kleptoplasty did not occur during first three weeks of benthic life. While larval growth rates and the nature of metamorphic cues are consistent with those of many other opisthobranch species with planktotrophic larvae, measures of post-larval growth—particularly as it pertains to kleptoplasty—is a new contribution to opisthobranch biology.


2008 ◽  
Vol 15 (5) ◽  
pp. 394-404 ◽  
Author(s):  
Stefan Scholz ◽  
Stephan Fischer ◽  
Ulrike Gündel ◽  
Eberhard Küster ◽  
Till Luckenbach ◽  
...  

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