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6. SETD2 safeguards the genome against isochromosome formation

Author

Mason, Frank M., primary, Kounlavong, Emily S., additional, Tebeje, Anteneh T., additional, Dahiya, Rashmi, additional, Guess, Tiffany, additional, Khan, Abid, additional, Vlach, Logan, additional, Norris, Stephen R., additional, Lovejoy, Courtney A., additional, Dere, Ruhee, additional, Strahl, Brian D., additional, Ohi, Ryoma, additional, Ly, Peter, additional, Walker, Cheryl Lyn, additional, and Rathmell, W. Kimryn, additional

Published
2023
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11. SETD2 safeguards the genome against isochromosome formation

Author

Mason, Frank M., primary, Kounlavong, Emily S., additional, Tebeje, Anteneh T., additional, Dahiya, Rashmi, additional, Guess, Tiffany, additional, Vlach, Logan, additional, Norris, Stephen R., additional, Lovejoy, Courtney A., additional, Dere, Ruhee, additional, Ohi, Ryoma, additional, Ly, Peter, additional, Walker, Cheryl L., additional, and Rathmell, W. Kimryn, additional

Published
2022
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23. Mutational analysis of TAF6 revealed the essential requirement of the histone‐fold domain and the HEAT repeat domain for transcriptional activation.

Author

Dahiya, Rashmi and Natarajan, Krishnamurthy

Subjects
*HISTONES, *GENETIC transcription, *GENETIC mutation, *IMMUNOPRECIPITATION, *AMINO acids
Abstract

TAF6, bearing the histone H4‐like histone‐fold domain (HFD), is a subunit of the core TAF module in TFIID and SAGA transcriptional regulatory complexes. We isolated and characterized several yeast TAF6 mutants bearing amino acid substitutions in the HFD, the middle region or the HEAT repeat domain. The TAF6 mutants were highly defective for transcriptional activation by the Gcn4 and Gal4 activators. CHIP assays showed that the TAF6‐HFD and the TAF6‐HEAT domain mutations independently abrogated the promoter occupancy of TFIID and SAGA complex in vivo. We employed genetic and biochemical assays to identify the relative contributions of the TAF6 HFD and HEAT domains. First, the temperature‐sensitive phenotype of the HEAT domain mutant was suppressed by overexpression of the core TAF subunits TAF9 and TAF12, as well as TBP. The HFD mutant defect, however, was suppressed by TAF5 but not by TAF9, TAF12 or TBP. Second, the HEAT mutant but not the HFD mutant was defective for growth in the presence of transcription elongation inhibitors. Third, coimmunoprecipitation assays using yeast cell extracts indicated that the specific TAF6 HEAT domain residues are critical for the interaction of core TAF subunits with the SAGA complex but not with TFIID. The specific HFD residues in TAF6, although required for heterodimerization between TAF6 and TAF9 recombinant proteins, were dispensable for association of the core TAF subunits with TFIID and SAGA in yeast cell extracts. Taken together, the results of our studies have uncovered the non‐overlapping requirement of the evolutionarily conserved HEAT domain and the HFD in TAF6 for transcriptional activation. [ABSTRACT FROM AUTHOR]

Published
2018
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25. Non-homologous end joining shapes the genomic rearrangement landscape of chromothripsis from mitotic errors.

Author

Hu Q, Valle-Inclan JE, Dahiya R, Guyer A, Mazzagatti A, Maurais EG, Engel JL, Cortés-Ciriano I, and Ly P

Abstract

Errors in mitosis can generate micronuclei that entrap mis-segregated chromosomes, which are susceptible to catastrophic fragmentation through a process termed chromothripsis. The reassembly of fragmented chromosomes by error-prone DNA double-strand break (DSB) repair generates a spectrum of simple and complex genomic rearrangements that are associated with human cancers and disorders. How specific DSB repair pathways recognize and process these lesions remains poorly understood. Here we used CRISPR/Cas9 to systematically inactivate distinct DSB processing or repair pathways and interrogated the rearrangement landscape of fragmented chromosomes from micronuclei. Deletion of canonical non-homologous end joining (NHEJ) components, including DNA-PKcs, LIG4, and XLF, substantially reduced the formation of complex rearrangements and shifted the rearrangement landscape toward simple alterations without the characteristic patterns of cancer-associated chromothripsis. Following reincorporation into the nucleus, fragmented chromosomes localize within micronuclei bodies (MN bodies) and undergo successful ligation by NHEJ within a single cell cycle. In the absence of NHEJ, chromosome fragments were rarely engaged by polymerase theta-mediated alternative end-joining or recombination-based mechanisms, resulting in delayed repair kinetics and persistent 53BP1-labeled MN bodies in the interphase nucleus. Prolonged DNA damage signaling from unrepaired fragments ultimately triggered cell cycle arrest. Thus, we provide evidence supporting NHEJ as the exclusive DSB repair pathway generating complex rearrangements following chromothripsis from mitotic errors., Competing Interests: STATEMENT OF COMPETING INTERESTS All authors have no competing interests to declare.

Published
2023
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