The genomic stability of the rDNA tandem array is tightly controlled to allow sequence homogenization and to prevent deleterious rearrangements. In this report, we show that the absence of the yeast CTD kinase I (CTDK-I) complex in null mutant strains leads to a decrease in the number of tandem rDNA repeats. Reintroduction of the missing gene induces an increase of rDNA repeats to reach a copy number similar to that of the original strain. Interestingly, while expansion is dependent on Fob1, a protein required for replication fork blocking activity in rDNA, contraction occurs in the absence of Fob1. Furthermore, silencing of class II genes at the rDNA, a process connected to rDNA stability, is not affected. Ctk1, the kinase subunit of the CTDK-I complex is involved in various steps of mRNA synthesis. In addition, we have recently shown that Ctk1 is also implicated in rRNA synthesis. The results suggest that the RNA polymerase I transcription defect occurring in a ctk1 mutant strain causes rDNA contraction.

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Journal Article | Research Support, Non-U.S. Gov't

Authors

Grenetier S, Bouchoux C, Goguel V

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