Ethanol exposure perturbs sea urchin development and disrupts developmental timing

Area of Science:

• Developmental Biology
• Teratology
• Marine Biology

Background:

• Ethanol is a known teratogen causing craniofacial defects in fetal alcohol syndrome (FAS).
• Sea urchin embryos offer a simplified model for studying skeletal patterning defects.

Purpose of the Study:

• To investigate the effects of ethanol on sea urchin embryonic development and skeletal patterning.
• To determine if known vertebrate FAS pathways are involved in ethanol's teratogenic effects in sea urchins.

Main Methods:

• Exposure of sea urchin embryos to ethanol.
• Analysis of skeletal morphology and gene expression.
• Temporal transcriptome analysis to assess global gene expression changes.

Main Results:

• Ethanol exposure induced broad skeletal patterning defects in sea urchin embryos.
• Ethanol disrupted the timing of developmental morphology and gene expression, including signaling and metabolic pathways.
• Key vertebrate FAS pathways (RA and Hh signaling) were not found to be responsible for ethanol's teratogenic effects in this model.

Conclusions:

• Ethanol's teratogenic effects in sea urchins stem from a disruption of temporal synchrony in gene expression networks.
• This loss of temporal synchrony between tissues underlies the observed skeletal patterning defects, offering insights into developmental disruptions.