[PDF] Effects of telomerase overexpression in the model organism Caenorhabditis elegans. | Semantic Scholar

Findings illustrate effects of telomere dysfunction in C. elegans mutants lacking the catalytic subunit of telomerase, trt-1, by identifying the 9–1–1 complex, a component of the Rad9/Rad1/Hus1 proliferating cell nuclear antigen–like sliding clamp, which may be required for telomerases to act at chromosome ends in C elegans.

It is found that telomere-length variation does not correlate with offspring production or longevity in C. elegans wild isolates, suggesting that naturally long telomeres play a limited role in modifying fitness phenotypes in Cournorhabditis elegans.

Caenorhabditis elegans with a mutation in the trt-1 telomerase reverse transcriptase gene is studied to speculate that telomersase is required to prevent or repair sporadic telomere truncations that are unrelated to the typical ‘end-replication’ problems.

A method that inserts a single copy of a transgene into a defined site and verified that single copies are inserted at the targeted site is developed.

The number of MosSCI insertion sites was expanded from two to six and three of the insertion sites led to robust expression in the germline from a ubiquitous promoter, which is important for expression in Improved Mos1-mediated transgenesis in C. elegans.

This new strain collection removes variation in the neuropeptide receptor gene npr-1, known to have large physiological and behavioral effects on C. elegans, and mitigates the hybrid strain incompatibility caused by zeel-1 and peel- 1, allowing for identification of quantitative trait loci that otherwise would have been masked by those effects.

It is shown that telomere length varies considerably in clonal populations of wild-type worms, and that these length differences are conserved over at least ten generations, suggesting a length regulation mechanism in cis.

Strong evidence is found that stochastic as well as genetic factors are significant in C. elegans ageing, with extensive variability both among same-age animals and between cells of the same type within individuals.

Depletion of TCAB1 by using RNA interference prevents TERC from associating with Cajal bodies, disrupts telomerase-telomere association, and abrogates telomere synthesis by telomersase.