Publications by authors named "Jane LaDu"
Article Synopsis
- The study focuses on the role of a specific long noncoding RNA, slincR, in how organisms respond to environmental toxins, specifically the compound TCDD which binds to the aryl hydrocarbon receptor (AHR).
- Researchers created a CRISPR-Cas9 mutant line of zebrafish with an altered slincR gene to investigate its biological functions, revealing that these mutant fish displayed increased sensitivity to TCDD, affecting their morphology and behavior.
- The findings indicate that the mutation in slincR disrupts metabolic pathways and cartilage development, and impairs the regenerative ability of the zebrafish, highlighting the lncRNA's crucial role in development and toxicological responses.
Ultraviolet-protective compounds, such as mycosporine-like amino acids (MAAs) and related gadusols produced by some bacteria, fungi, algae, and marine invertebrates, are critical for the survival of reef-building corals and other marine organisms exposed to high-solar irradiance. These compounds have also been found in marine fish, where their accumulation is thought to be of dietary or symbiont origin. In this study, we report the unexpected discovery that fish can synthesize gadusol de novo and that the analogous pathways are also present in amphibians, reptiles, and birds.
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- * Researchers found that knocking down otoferlin in zebrafish led to hearing and coordination issues, as well as problems with swim bladders, indicating its critical role in these functions.
- * The study demonstrated that full-length and certain truncated forms of otoferlin could restore hearing and balance in the affected zebrafish, highlighting the evolutionary importance of this protein in vertebrates.
Pseudoloma neurophilia (Microsporidia) is very common in zebrafish Danio rerio research facilities. A new zebrafish facility has been established at the Sinnhuber Aquatic Resource Laboratory (SARL), Oregon State University, Corvallis, OR, U.S.
View Article and Find Full Text PDFExposure to dioxins, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), causes a wide array of toxicities in vertebrates, which are mostly considered to be mediated through the inappropriate activation of the aryl hydrocarbon receptor (AHR) signaling pathway. Although transcriptional regulation by AHR is widely studied, the molecular mechanisms responsible for the adverse outcomes after AHR activation are largely unknown. To identify the important downstream events of AHR activation, we employed the zebrafish caudal fin regeneration model, where AHR activation blocks the regenerative process.
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