Heterochromatin transcription and alternative chromosome end-protection mechanisms in the absence of canonical telomeres


Session type:

Martina Begnis1, Julie Cooper1
1Cancer Research UK London Research Institute, London, UK


The discovery of HAATI chromosomes in fission yeast has recently shaken the dogma that canonical telomeres are essential to maintain chromosome linearity. HAATI cells survive telomerase loss by rearranging the genome such that blocks of genetric heterochromatin jump to the ends of chromosomes and acquire the ability to recruit the canonical end protection factor Pot1. These survivors amplify either of two classes of repetitive sequences, the rDNA for rDNA-HAATI and the subtelomeric repeats for STE-HAATI.


Southern blot; Pulsed-field gel electrophoresis.


RNAi is one of the pathways that contribute to the formation of heterochromatin in the genome, however it is dispensable for the establishment of heterochromatin at canonical telomeres.

Here we show that small non-coding RNAs are required for the jumping of rDNA repeats that allows the formation of rDNA-HAATI. On the contrary, STE-HAATI generation appears to be actively promoted by the loss of Dicer (Dcr1) but not Argonaute (Ago1), both actors of the RNAi pathway.

Interestingly, the role of Dcr1 and Ago1 is critical for the formation of HAATI chromosomes but is not essential for their maintenance.


Our results implicate heterochromatin transcription in the formation of specific types of alternative chromosome end-protection complexes. These complexes are reminiscient of Drosophila telomeres and might be widely conserved, for instance in human telomerase-minus cancer cells.

We propose that Dcr1 might play a role in repressing those mechanisms that affect STE mobility, possibly involving transposition-like events.