Project description:The majority of Saccharomyces cerevisiae snoRNA promoters contain an aRCCCTaa sequence motif located at the upstream border of a TATA-containing nucleosome-free region. Genome-wide ChIP-seq analysis showed that these motifs are bound in vivo by Tbf1, a telomere-binding protein known to recognize mammalian-like T2AG3 repeats at sub-telomeric regions. Tbf1 has over 100 additional promoter targets, including the TBF1 gene itself. Tbf1 is required for full snoRNA expression, yet it does not influence nucleosome positioning at snoRNA promoters. Analysis of Tbf1-binding sites in Saccharomyces cerevisiae by ChIP-seq of a Myc-tagged strain and a control untagged strain. 1 sample per strain, 1 lane per sample.
Project description:The majority of Saccharomyces cerevisiae snoRNA promoters contain an aRCCCTaa sequence motif located at the upstream border of a TATA-containing nucleosome-free region. Genome-wide ChIP-seq analysis showed that these motifs are bound in vivo by Tbf1, a telomere-binding protein known to recognize mammalian-like T2AG3 repeats at sub-telomeric regions. Tbf1 has over 100 additional promoter targets, including the TBF1 gene itself. Tbf1 is required for full snoRNA expression, yet it does not influence nucleosome positioning at snoRNA promoters.
Project description:In Saccharomyces cerevisiae, the kinase Rio1 regulates rDNA transcription and segregation, pre-rRNA cleavage, and 40S ribosomal subunit maturation. Other roles are unknown. Human orthologue RIOK1; which is frequently overexpressed in malignancies, drives tumor growth and metastasis. Again, also RIOK1 biology is poorly understood. In this study, we charted the global activity of Rio1 in budding yeast. By producing and systems-integrating its protein-interaction, gene-transcription, and chromatin-binding maps we generated Rio1's multi-layered activity network, which controls protein synthesis and turnover, metabolism, growth, proliferation, and genetic stability. Rio1 regulates itself at the transcriptional level, and manages its network both directly and indirectly, via a battery of regulators and transcription factors, including Gcn4. We experimentally confirmed the network and show that Rio1 commands its downstream circuit depending on the growth conditions encountered. We also find that Rio1 and RIOK1 activities are functionally equivalent. Our data suggest that pathological RIOK1 expression may deregulate its network and fuel promiscuous transcription and ribosome production, uncontrolled metabolism, growth, proliferation, and chromosomal instability; well-known contributors to cancer initiation, maintenance and metastasis.