Involvement of aberrant chromosome architecture and locus-specific vulnerability to DNA methylation epimutations in bovine large offspring syndrome
Abstract
Large/abnormal offspring syndrome (LOS/AOS) and Beckwith-Wiedemann syndrome (BWS) are similar congenital overgrowth syndromes which occur naturally in ruminants and humans, respectively. The incidence of these syndromes increases when offspring are conceived with the use of assisted reproductive technologies (ART; i.e. in vitro oocyte maturation, in vitro fertilization, and embryo culture). Molecular defects reported in both syndromes include global gene misregulation, DNA methylome epimutations, and disruption of genomic imprinting (parental-allele-specific gene expression). Although we have reported that bovine LOS occurs spontaneously (SLOS) based on phenotypic similarities to ART-LOS, to date no study has been conducted to determine if SLOS has the same methylome epimutations as ART-LOS. One goal of my dissertation research is to characterize DNA methylation profiles in bovine SLOS and ART-LOS to determine whether there are conserved genomic loci with DNA methylation defects between these overgrowth conditions. In addition, while it is known that LOS is characterized by global alterations in DNA methylation, it is largely unknown how altered DNA methylation drives the development of LOS, as the methylation errors (i.e., differentially methylated regions; DMRs) observed in the syndrome only explain [less than] 4 percent of the gene misregulation in short range (the flanking 20,000 DNA bases from the DMR). Therefore, another goal of my dissertation research is to determine…
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