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Related Experiment Video

Updated: Nov 17, 2025

Analysis of Oxidative Stress in Zebrafish Embryos

Analysis of Oxidative Stress in Zebrafish Embryos

Published on: July 7, 2014

Vitamin E Deficiency Disrupts Gene Expression Networks during Zebrafish Development.

Brian Head^1,2, Stephen A Ramsey^3,4, Chrissa Kioussi⁵

¹Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.

|February 12, 2021

Summary

This summary is machine-generated.

Embryonic Vitamin E (VitE) deficiency causes widespread gene expression disruption, impacting metabolism and development from early stages. This leads to significant developmental issues and ultimately lethal outcomes in zebrafish embryos.

Keywords:

E+, VitE sufficient E–, VitE deficient VitE hours post-fertilization hpf vitamin E α-TTP α-tocopherol transfer protein.

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Last Updated: Nov 17, 2025

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Area of Science:

Developmental Biology
Genetics
Nutritional Science

Background:

Vitamin E (VitE) is crucial for vertebrate embryogenesis.
The precise molecular mechanisms underlying VitE's role in embryonic development are not fully understood.

Purpose of the Study:

To investigate the transcriptional basis of metabolic and phenotypic outcomes in zebrafish embryos with Vitamin E deficiency.
To identify early molecular changes associated with embryonic VitE deficiency.

Main Methods:

Zebrafish adults were fed either Vitamin E sufficient (E+) or deficient (E-) diets.
Embryos from these fish were collected at 12, 18, and 24 hours post-fertilization (hpf).
Gene expression profiling was performed using RNASeq, followed by hierarchical clustering and enrichment analyses.

Main Results:

Vitamin E deficient (E-) embryos exhibited significant disruption in gene expression.
Affected pathways included gene transcription, carbohydrate and energy metabolism, intracellular signaling, and embryonic structure formation.
The mechanistic target of rapamycin (mTOR) pathway was identified as a key regulator of these changes.

Conclusions:

Embryonic Vitamin E deficiency causes genetic and transcriptional dysregulation as early as 12 hpf.
This dysregulation leads to metabolic dysfunction and severe developmental defects.
Vitamin E deficiency has ultimately lethal outcomes for developing zebrafish embryos.