Abstract

Over 15 million babies have been conceived by IVF, yet debate about its safety to offspring continues. We hypothesized that superovulation and in vitro fertilization (IVF) promote genomic changes, including altered telomere length (TL) and activation of the retrotransposon LINE-1 (L1), and tested this hypothesis in a mouse model.

Highlights

  • Telomeres are non-coding, repetitive DNA sequences of TTAGGG located at the termini of linear chromosomes [1]

  • L1 copy number of blastocysts cultured for 120 hours (n=15, Mean: 1.71± 1.49) exceeded that of embryos cultured for 96 hours (n=67, Mean: 0.95 ± 1.03; p=0.0162)

  • Intriguingly ovarian stimulation, alone or followed by in vitro fertilization (IVF), produced embryos with significantly longer telomeres compared to in vivo, natural cycle-produced embryos. The significance of this enriched telomere endowment for the health and longevity of offspring born from IVF merit future studies

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Summary

Introduction

Telomeres are non-coding, repetitive DNA sequences of TTAGGG located at the termini of linear chromosomes [1] It protects the end of chromosomes by forming single strands that invade the telomeric double helix to create loops, called t-loops. Telomere length (TL) shortens due to the inability of the DNA polymerase enzyme to complete synthesis if the lagging strand at chromosomal ends [3]. When cells divide, they cannot replicate approximately 50 base pairs of the lagging DNA strand at chromosome ends [4]. This limits the number of divisions that a cell can tolerate because when telomeres reach a critical size, senescence and programmed cell death occur [5]

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