Chronic sublethal exposure to methylmercury lengthens telomeres in developing zebra finches.

Methylmercury (MeHg) is a widespread environmental pollutant known to cause DNA and chromosomal damage, in part through reactive oxygen species (ROS). Telomeres, essential for chromosomal protection, are highly sensitive to oxidative damage and consequent shortening. While ROS-dependent oxidative stress accelerates telomere attrition in vitro, the mechanisms by which chronic exposure to ROS-inducing exogenous agents affects telomere length in vivo remain unclear. We studied effects of sublethal, multi-generational MeHg exposure on telomere dynamics during early life in zebra finches (Taeniopygia guttata). Continuous exposure to an environmentally relevant concentration of dietary MeHg (1.2 mg/kg) resulted in longer relative telomeres in red blood cells, brain, liver, kidney and lung by sexual maturity. No evidence of selection for longer telomeres across generations of MeHg exposure was observed. Lung protein expression of proliferating cell nuclear antigen (PCNA), a DNA synthesis marker, remained unchanged, suggesting telomere maintenance or elongation occurs independently of proliferation. However, β-Catenin expression, a key transcription factor in Wnt signaling, increased in young MeHg-exposed birds. Transcriptomic analysis of bone marrow revealed up-regulation of oncogenic and pro-inflammatory signaling pathways and down-regulation of mitotic cell cycle pathways. Combined, our data reveal cellular processes reminiscent of tumorigenesis and suggestive of replicative immortality of telomeres under chronic stress.