Telomeres protect and cap linear chromosome ends, yet these genomic buffers erode over an organism's lifespan. Short telomeres have been associated with many age-related conditions in humans, and genetic mutations resulting in short telomeres in humans manifest as syndromes of precocious aging. In women, telomere length limits a fertilized egg's capacity to develop into a healthy embryo. Thus, telomere length must be reset with each subsequent generation. Although telomerase is purportedly responsible for restoring telomere DNA, recent studies have elucidated the role of alternative telomeres lengthening mechanisms in the reprogramming of early embryos and stem cells, which we review here.
in 10 mM AZT treated embryos, while miR-34a change was not significant in the 1mM AZT treatment group.CONCLUSIONS: AZT, which disrupts early development and inhibits telomere elongation in early embryos, alters expression of a number of miRNAs previously shown to regulate telomere dynamics. Our results also show AZT increases expression of mir34a, which is known to be an inhibitor of totipotency. The relationships among telomere length, miRNA expression, and embryo development need further investigation, both to identify potentially long term effects of prenatal exposure to AZT, and to elucidate the biology of early human development.References: 1. Philipp et al, The Journal of Infectious Diseases 1991;163:1212-1218. 2. Fischl MA, Richman DD, Grieco MH, et al. The efficacy of azidothymidine (AZT) in the treatment of patients with AIDS and AIDSrelated complex: a double-blind, placebo-controlled trial.
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