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Publication of UMR8226

Publication of UMR8226

Publication of team Telomere Biology in Genes & Development

Adaptation to DNA damage checkpoint in senescent telomerase-negative cells promotes genome instability. Genes & Dev. 32:1–15. [Supp]

Coutelier H*, Xu Z*#, Morisse MC,  Lhuillier-Akakpo M, Pelet S, Charvin G, Dubrana K and TeixeiraMT #. (2018).

#Corresponding authors

*These authors contributed equally to this work.

 

Telomere shortening limits cell proliferation by triggering the DNA damage checkpoint, arresting the cells in replicative senescence. However, time-resolved single-cell analysis of telomerase-negative yeast cells reveals that they also experience nonpermanent arrests followed by additional cell divisions before terminal senescence. Careful monitoring of the DNA damage checkpoint is thus critical to understand the senescence process. Illustrated here is a fluorescent reporter to assess checkpoint activation, composed of a nuclear marker (Hta2-yECFP; cyan) and an artificial construct made by the FHA1 domain of Rad53 fused to mCherry (FHA1-mCherry; red). FHA1-mCherry translocates to the nucleus to interact with the checkpoint adaptor Rad9 if the cell experiences DNA damage. In the right panel are shown cells challenged by the DNA damage-inducing agent zeocin, with the FHA1-mCherry enriched in the nucleus, and the merge appearing yellow. In the left panel, similarly challenged cells express a mutant version of the reporter FHA1-H75A-mCherry, which is no longer able to interact with Rad9 (the nucleus is now cyan), demonstrating the specificity of the reporter. (For details, see Coutelier et al., p. 1499.)


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