Vitamin E Deficiency Disrupts Gene Expression Networks during Zebrafish Development.

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.