Dear James and Everyone, Sadly I couldn’t open much of what you attached. I’m pretty aware of most of what you say when you say, ” of what controls telomeres, which includes long non-coding RNA (TERRA), histone trimethylation (H3K9 and H4K20), COMPASS (H3K4me3), histone H3K79 trimethylation, histone hyperacetylation, Rb proteins, subtelomeric DNA methylation (DNMTs), the miR-290 family, Shelterin proteins, Rap-1, SIRT1, Tankyrases, SIRT6, and the ALT mechanism are all very important aspects of telomere length control.” I agree those mechanisms may be very important in establishing telomere length at various time during the organism’s lifespan, but I am at this point past the mechanics of the intracellular processes, I’m concerned with what controls them – and I believe that it is the body that communicates with its cells in such a way as to establish the cellular age phenotype peculiar to various post-adult life stages – the cell conforms using the mechanisms (mostly epigenetic) you mention to control those various aspects that make up cellular age-phenotype. As Steve Hill observed – the greatest likelihood is that blood-borne signals act to change epigenetic patterns changing the histone code, DNA methylation patterns, restricting translation with miRNAs etc. at the behest of the body – not an unfolding program in the cells themselves, but an unfolding program of the body as a whole. So yes, you can see there are many controls over and effects of telomere length – but the mere fact that it CAN be controlled by the cell, that it can lengthened at “will” – means that the choice to not lengthen it is just that. The cell does not make such choices on its own (except in the case of cancers).
I am however intrigued by tankarases that make PARP figure into both DNA repair and telomere length regulation – I’ve found some articles.