Chronic Exposure to a Sublethal Concentration of Methyl-Mercury Early in Life Affects Telomere Dynamics and Genomic Stability in Zebra Finches
Telomeres are essential for chromosomal protection, yet their guanine-rich repeats are sensitive to oxidative damage. ROS-dependent oxidative stress accelerates telomere attrition in vitro, but telomere dysfunction under oxidative conditions in vivo remains unclear. We studied the effects of ROS-inducing agent methyl-mercury (MeHg) on telomere and genome dysfunction in zebra finches (Taeniopygia guttata). Using qPCR, we found that continuous exposure to sublethal MeHg (1.2 ppm in the diet) resulted in longer telomere length than controls by sexual maturity in red blood cells and several other tissues. These findings were accompanied by suppressed bone marrow transcriptomic pathways related to cilia formation and mitotic progression. Further analysis revealed oncogenic and pro-inflammatory signaling reminiscent of tumorigenesis. We also demonstrate that PCNA expression in the lung remains unchanged by MeHg, suggesting telomere maintenance independent of replication. Our results show that chronic sublethal MeHg exposure may lead to replicative immortality of telomeres rather than shortening. Overall design: To investigate the impact of a sublethal dosage of MeHg (1.2 ppm in food) on the hematopoietic system, we bred zebra finches of varied historical exposure and performed gene expression profiling analyses, alongside gene set enrichment analysis using data obtained from RNA-seq of 4 different developmental time points.