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Long-Read Isoform Sequencing Reveals Aroclor1260-Induced Isoform Usage in Mouse Livers
Belinda J Petri1,2,3, Kellianne M Piell1, Banrida Wahlang4,5,6
1Department of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Genes
|February 27, 2026
Summary
Polychlorinated biphenyls (PCBs) exposure causes metabolic dysfunction-associated steatotic liver disease (MASLD). Long-read sequencing reveals PCBs alter gene transcript usage, impacting key metabolic pathways in the liver.
Area of Science:
- Environmental toxicology
- Molecular biology
- Hepatology
Background:
- Long-term exposure to polychlorinated biphenyls (PCBs), such as Aroclor1260 (Ar1260), induces metabolic dysfunction-associated steatotic liver disease (MASLD).
- While gene expression changes are known, the roles of alternative splicing (AS) and differential transcript usage (DTU) in PCB-induced MASLD remain unclear.
- Previous work identified hepatic RNA modifications and altered selenoprotein levels following chronic Ar1260 exposure in mice.
Purpose of the Study:
- To investigate the impact of Ar1260 exposure on alternative splicing and differential transcript usage in mouse liver.
- To identify specific genes and pathways affected by PCB-induced DTU in the context of MASLD.
Main Methods:
- Utilized long-read isoform sequencing (IsoSeq) to analyze transcriptomes from Ar1260-exposed mouse livers.
- Focused on identifying DTU in four key genes: Adpgk, Blvra, Mup2, and Ndufaf6.
- Performed network analysis on the proteins encoded by these differentially spliced genes.
Main Results:
- Identified differential transcript usage in Adpgk, Blvra, Mup2, and Ndufaf6 in response to Ar1260 exposure.
- Network analysis linked the proteins from these genes to critical MASLD-related pathways, including lipid metabolism, glycolysis, and oxidative stress.
Conclusions:
- PCB exposure significantly alters the landscape of transcript isoforms for crucial metabolic genes.
- These alterations in transcript usage are associated with key molecular pathways implicated in the development of MASLD.
