Does telomere dysfunction play a role in embryo arrest?
The signaling of permanent cell cycle arrest has long been attributed to the critical shortening of telomere(s), the repetitive DNA sequences (TTAGGG)n and associated proteins located at the ends of mammalian chromosomes (Harley et al., 1990, 1992; Allsopp et al., 1992, 1995; Vaziri, 1997; Vaziri and Benchimol, 1998). Telomere shortening can be overcome by the de novo synthesis of telomeric DNA by telomerase (Greider and Blackburn, 1985), a multi-subunit reverse transcriptase that uses its RNA component (TERC) to align itself to the chromosomal ends and as a template for the synthesis of telomeric sequences (Collins and Greider, 1995; Collins et al., 1995). High levels of telomerase activity have been detected in germ line tissues, cells of renewal tissues, cancer cells and immortalized cell lines but not in most somatic tissues (Kim et al., 1994; Harle-Bachor and Boukamp, 1996; Wright et al., 1996; Betts and King, 1999). Ectopic expression of the telomerase catalytic subunit (TERT) ex
