Genetically encoded thiol redox-sensors in the zebrafish model: lessons for embryonic development and regeneration.

Biol Chem

Institute of Biological and Chemical Systems - Biological Information Processing, Karlsruhe Institute of Technology, Hermann-von-Helmholtz-Platz 1, D-76344Eggenstein-Leopoldshafen, Germany.

Published: February 2021


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Important roles for reactive oxygen species (ROS) and redox signaling in embryonic development and regenerative processes are increasingly recognized. However, it is difficult to obtain information on spatiotemporal dynamics of ROS production and signaling . The zebrafish is an excellent model for bioimaging and possesses a remarkable regenerative capacity upon tissue injury. Here, we review data obtained in this model system with genetically encoded redox-sensors targeting HO and glutathione redox potential. We describe how such observations have prompted insight into regulation and downstream effects of redox alterations during tissue differentiation, morphogenesis and regeneration. We also discuss the properties of the different sensors and their consequences for the interpretation of imaging results. Finally, we highlight open questions and additional research fields that may benefit from further application of such sensor systems in zebrafish models of development, regeneration and disease.

Download full-text PDF

Source
http://dx.doi.org/10.1515/hsz-2020-0269DOI Listing

Publication Analysis

Top Keywords

genetically encoded
8
embryonic development
8
development regeneration
8
encoded thiol
4
thiol redox-sensors
4
redox-sensors zebrafish
4
zebrafish model
4
model lessons
4
lessons embryonic
4
regeneration roles
4

Similar Publications

modulates presynaptic Ca1.3 Ca channel function in inner hair cells (IHCs) and is required for indefatigable synaptic sound encoding. Biallelic variants in are associated with non-syndromic hearing loss (DFNB93).

View Article and Find Full Text PDF

MAGIS syndrome: phenotypes, pathogenesis, and treatment.

J Hum Immun

November 2025

Human Immunological Diseases Section, Laboratory of Clinical Immunology and Microbiology, Intramural Research Program, NIAID, NIH, Bethesda, MD, USA.

Inborn errors of immunity (IEI) presenting with immunodeficiency and autoimmunity can illuminate pathways essential for immunocompetence and self-tolerance. We recently characterized a new IEI named MAGIS ("idline malformations of the brain, nterior pituitary gland dysfunction, rowth retardation, mmunodysregulation/immunodeficiency, and keletal defects") caused by heterozygous germline activating mutations in (encoding the heterotrimeric G-protein, G). This disorder demonstrates the central role of G regulation of chemotaxis in humans and a novel pathway by which G-proteins regulate T-cell activation.

View Article and Find Full Text PDF

Background: Most RNA-seq datasets harbor genes with extreme expression levels in some samples. Such extreme outliers are usually treated as technical errors and are removed from the data before further statistical analysis. Here we focus on the patterns of such outlier gene expression to investigate whether they provide insights into the underlying biology.

View Article and Find Full Text PDF

Retinitis pigmentosa (RP) affects around 1 in 4000 individuals and represents approximately 25% of cases of vision loss in adults, through death of retinal rod and cone photoreceptor cells. It remains a largely untreatable disease, and research is needed to identify potential targets for therapy. Mutations in 94 different genes have been identified as causing RP, including AGBL5 which encodes the main deglutamylase that regulates and maintains functional levels of cilia tubulin glutamylation, which is essential to initiate ciliogenesis, maintain cilia stability and motility.

View Article and Find Full Text PDF

Several genes in the mitochondria of angiosperms are interrupted by introns, and their posttranscriptional excision involves numerous nucleus-encoded auxiliary factors. Most of these factors are of eukaryotic origin, among them members of the pentatricopeptide-repeat (PPR) family of RNA-binding proteins. This family divides into the PLS and P classes, with PLS-class proteins typically participating in C-to-U mRNA editing and P-class members contributing to transcript stabilization and intron splicing.

View Article and Find Full Text PDF