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Related Experiment Video

Updated: Jan 10, 2026

Rapid Identification of Chemical Genetic Interactions in Saccharomyces cerevisiae

Rapid Identification of Chemical Genetic Interactions in Saccharomyces cerevisiae

Published on: April 5, 2015

Mapping Chemical-Gene Interactions for Developmental Lethality and Pregnancy Loss.

Syed Hassan Bukhari¹, Amrita Nagasuri¹, Boris Oskotsky¹

¹Bakar Computational Health Sciences Institute, University of California, San Francisco, CA, USA.

Medrxiv : the Preprint Server for Health Sciences

|November 24, 2025

Summary

This summary is machine-generated.

Environmental exposures can cause pregnancy loss by disrupting critical genes during development. The Chemical-Gene Atlas (CGA) tool helps identify these chemical-gene interactions and vulnerable developmental periods.

Keywords:

Chemical-Gene Interactions Developmental Lethality Exposomics Pregnancy Loss Recurrent Pregnancy Loss (RPL)

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Published on: June 17, 2015

Area of Science:

Reproductive toxicology
Developmental biology
Environmental health

Background:

Pregnancy loss impacts 10-15% of pregnancies, influenced by genetic and environmental factors.
Existing resources lack organization for chemical-gene interactions by gestational timing, maternal-fetal compartment, or lethality context.

Purpose of the Study:

To bridge the gap in understanding chemical-gene interactions related to pregnancy loss.
To develop a resource organizing chemical-gene evidence by developmental context.

Main Methods:

Merged Intolerome genes and Comparative Toxicogenomics Database data.
Created a network of 928 lethality-associated genes and ~4,000 chemicals.
Developed the Chemical-Gene Atlas (CGA) application with four filters for hypothesis generation and clinical translation.

Main Results:

Identified five clinically important genes (F5, F2, AURKB, PADI6, FOXD1) associated with recurrent pregnancy loss (RPL).
Demonstrated differential exposomic patterns of Bisphenol A (BPA) and Benzo[a]pyrene (B[a]P) affecting these genes.
Showcased disruption of gene expression, methylation, coagulation pathways, and placental function.

Conclusions:

Genes with loss-of-function intolerance, particularly in metabolic and cardiovascular systems, are susceptible to environmental disruption.
Environmental exposures impact critical developmental windows like implantation, placental development, and early organogenesis.
The CGA platform offers a scalable model for investigating chemical-gene interactions causing developmental lethality.