Gene Expression Analysis of the Stress Response to Lithium, Nickel, and Zinc in Paracentrotus lividus Embryos.
Rosa BonaventuraCaterina CostaIrene DeiddaFrancesca ZitoRoberta RussoPublished in: Toxics (2022)
Many anthropogenic pollutants such as metals are discharged into the marine environment through modern sources. Among these, lithium (Li), nickel (Ni), and zinc (Zn) can interfere with biological processes in many organisms when their concentration rises. These metals are toxic to sea urchin embryos, affecting their development. Indeed, animal/vegetal and dorso/ventral embryonic axes are differently perturbed: Li is a vegetalizing agent, Ni can disrupt dorso-ventral axis, Zn can be animalizing. To address the molecular response adopted by embryos to cope with these metals or involved in the gene networks regulating embryogenesis, and to detect new biomarkers for evaluating hazards in polluted environments in a well-known in vivo model, we applied a high-throughput screening approach to sea urchin embryos. After fertilization, Paracentrotus lividus embryos were exposed to Li, Ni, and Zn for 24/48 h. At both endpoints, RNAs were analyzed by NanoString nCounter technology. By in silico analyses, we selected a panel of 127 transcripts encoding for regulatory and structural proteins, ranked in categories: Apoptosis, Defense, Immune, Nervous, Development, and Biomineralization. The data analysis highlighted the dysregulation of many genes in a metal-dependent manner. A functional annotation analysis was performed by the KEEG Orthology database. This study provides a platform for research on metals biomarkers in sea urchins.
Keyphrases
- heavy metals
- health risk assessment
- health risk
- data analysis
- human health
- gene expression
- oxide nanoparticles
- solid state
- metal organic framework
- risk assessment
- spinal cord
- ion batteries
- genome wide identification
- genome wide
- drinking water
- deep brain stimulation
- emergency department
- transcription factor
- copy number
- endoplasmic reticulum stress
- cell death
- prefrontal cortex
- cell cycle arrest
- spinal cord injury
- innate immune