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#telomeres

2 public questions tagged with this topic.

Eukaryotes gene regulation

Telomeric silencing in yeast spreads due to:

Telomeric position effect in budding yeast involves Sir complex spreading from chromosome ends inward silencing subtelomeric genes. Rap1 protein binds TG1-3 telomere repeats recruiting Sir4 which interacts with Sir2 histone deacetylase. Sir2 deacetylates adjacent nucleosomal H4K16 and H3K9, generating high-affinity binding site for Sir3 chromodomain interacting with deacetylated tails, recruiting additional Sir2-Sir4 complexes iteratively propagating heterochromatin several kilobases. This histone deacetylation dependent polymerization requires continuous Sir2 NAD-dependent activity, blocked by boundary elements or acetyltransferases. Disruption of deacetylation restores acetylation evicting Sir proteins activating normally silent loci, illustrating requirement for histone deacetylation in spreading and maintenance of telomeric heterochromatin inheritance.

Ref: Lodish et al., Molecular Cell Biology, 9th ed., Chapter 8: Telomeric Silencing Spread via Histone Deacetylation

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Transposable elements

End replication problem is solved by

End replication problem arises because DNA polymerases require primer and synthesize only 5' to 3', leaving lagging strand telomere unable to be fully replicated after removal of terminal RNA primer. Telomerase overcomes this by specialized ribonucleoprotein containing intrinsic RNA template complementary to telomeric repeat and protein reverse transcriptase subunit TERT that extends 3' G-rich overhang adding TTAGGG repeats in humans. Extension creates substrate for primase-pol alpha fill-in of complementary C-rich strand, maintaining telomere length, preventing senescence, and supporting immortalization of germline and cancer cells.

Ref: Lodish et al., Molecular Cell Biology, 9th ed., Chapter 11: Telomerase Solves End Replication Problem

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