Set5 and Set1 cooperate to repress gene expression at telomeres and retrotransposons

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dc.contributor.authorMartín, Glòria Mas
dc.contributor.authorKing, Devin A
dc.contributor.authorGreen, Erin
dc.contributor.authorGarcia-Nieto, Pablo E
dc.contributor.authorAlexander, Richard
dc.contributor.authorCollins, Sean R
dc.contributor.authorKrogan, Nevan J
dc.contributor.authorGozani, Or P
dc.contributor.authorMorrison, Ashby J
dc.date.accessioned2023-01-25T15:08:38Z
dc.date.available2023-01-25T15:08:38Z
dc.date.issued2014-01-17
dc.description.abstractA complex interplay between multiple chromatin modifiers is critical for cells to regulate chromatin structure and accessibility during essential DNA-templated processes such as transcription. However, the coordinated activities of these chromatin modifiers in the regulation of gene expression are not fully understood. We previously determined that the budding yeast histone H4 methyltransferase Set5 functions together with Set1, the H3K4 methyltransferase, in specific cellular contexts. Here, we sought to understand the relationship between these evolutionarily conserved enzymes in the regulation of gene expression. We generated a comprehensive genetic interaction map of the functionally uncharacterized Set5 methyltransferase and expanded the existing genetic interactome of the global chromatin modifier Set1, revealing functional overlap of the two enzymes in chromatin-related networks, such as transcription. Furthermore, gene expression profiling via RNA-Seq revealed an unexpected synergistic role of Set1 and Set5 in repressing transcription of Ty transposable elements and genes located in subtelomeric regions. This study uncovers novel pathways in which the methyltransferase Set5 participates and, more importantly, reveals a partnership between Set1 and Set5 in transcriptional repression near repetitive DNA elements in budding yeast. Together, our results define a new functional relationship between histone H3 and H4 methyltransferases, whose combined activity may be implicated in preserving genomic integrity.en_US
dc.description.sponsorshipThe authors wish to thank the members of the Morrison, Gozani, and Chua labs for helpful discussions and critical reading of the manuscript. We thank A. Morillon (Institut Curie Paris) for generously providing yeast strains. We are grateful for the guidance and RNA-Seq reagents supplied by the Lab of Hunter Fraser at Stanford University, and the services provided by the Protein and Nucleic Acid facility at Stanford University. Martín GM was supported by the Generalitat de Catalunya Beatriu de Pinós award BP-A 2010. Morrison AJ is supported by funding from NIH (R00 GM085212). This work was supported in part by a grant from the NIH to Gozani O (R01 CA172560). Gozani O is a recipient of an Ellison Senior Scholar in Aging Award.en_US
dc.description.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121362/en_US
dc.format.extent10 pagesen_US
dc.genrejournal articlesen_US
dc.identifierdoi:10.13016/m2vyyn-nibt
dc.identifier.citationMartín, Glòria Mas et al. “Set5 and Set1 cooperate to repress gene expression at telomeres and retrotransposons.” Epigenetics vol. 9,4 (2014): 513-22. doi:10.4161/epi.27645en_US
dc.identifier.urihttps://doi.org/10.4161%2Fepi.27645
dc.identifier.urihttp://hdl.handle.net/11603/26702
dc.language.isoen_USen_US
dc.publisherTaylor & Francisen_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Biological Sciences Department Collection
dc.rightsThis item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.en_US
dc.subjecttranscriptionen_US
dc.subjectgenetic interactionen_US
dc.subjectSet5en_US
dc.subjectSet1en_US
dc.subjecthistone methylationen_US
dc.subjecttelomeresen_US
dc.subjectretrotransposonsen_US
dc.titleSet5 and Set1 cooperate to repress gene expression at telomeres and retrotransposonsen_US
dc.typeTexten_US
dcterms.creatorhttps://orcid.org/0000-0003-3923-6726en_US

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