H3.1K27me1 maintains transcriptional silencing and genome stability by preventing GCN5-mediated histone acetylation (Record no. 52916)
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| fixed length control field | 02371nam a2200277Ia 4500 |
| 003 - CONTROL NUMBER IDENTIFIER | |
| control field | MX-MdCICY |
| 005 - DATE AND TIME OF LATEST TRANSACTION | |
| control field | 20250625162418.0 |
| 040 ## - CATALOGING SOURCE | |
| Transcribing agency | CICY |
| 090 ## - LOCALLY ASSIGNED LC-TYPE CALL NUMBER (OCLC); LOCAL CALL NUMBER (RLIN) | |
| Classification number (OCLC) (R) ; Classification number, CALL (RLIN) (NR) | B-18770 |
| 008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION | |
| fixed length control field | 250602s9999 xx |||||s2 |||| ||und|d |
| 245 10 - TITLE STATEMENT | |
| Title | H3.1K27me1 maintains transcriptional silencing and genome stability by preventing GCN5-mediated histone acetylation |
| 490 0# - SERIES STATEMENT | |
| Volume/sequential designation | The Plant Cell, 33, p.961-979, 2021 |
| 520 3# - SUMMARY, ETC. | |
| Summary, etc. | pigenetic mechanisms play diverse roles in the regulation of genome stability in eukaryotes. In Arabidopsis thaliana, genome stability is maintained during DNA replication by the H3.1K27 methyltransferases ARABIDOPSIS TRITHORAXRELATED PROTEIN 5 (ATXR5)and ATXR6, which catalyze the deposition of K27me1 on replication-dependent H3.1 variants. The loss of H3.1K27me1 in atxr5 atxr6 double mutants leads to heterochromatin defects, including transcriptional de-repression and genomic instability, but the molecular mechanisms involved remain largely unknown. In this study, we identified the transcriptional co-activator and conserved histone acetyltransferase GCN5 as a mediator of transcriptional de-repression and genomic instability in the absence of H3.1K27me1. GCN5 is part of a SAGA-like complex in plants that requires the GCN5-interacting protein ADA2b and the chromatin remodeler CHR6 to mediate the heterochromatic defects in atxr5 atxr6 mutants. Our results also indicate that Arabidopsis GCN5 acetylates multiple lysine residues on H3.1 variants, but H3.1K27 and H3.1K36 play essential functions in inducing genomic instability in the absence of H3.1K27me1. Finally, we show that H3.1K36 acetylation by GCN5 is negatively regulated by H3.1K27me1 in vitro. Overall, this work reveals a key molecular role for H3.1K27me1 in maintaining transcriptional silencing and genome stability in heterochromatin by restricting GCN5-mediated histone acetylation in plants. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Jie Dong |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Chantal Leblanc |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Axel Poulet |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Benoit Mermaz |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Gonzalo Villarino |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Kimberly M. Webb |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Valentin Joly |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Valentin Joly |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Philipp Voigt |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Yannick Jacob |
| 856 40 - ELECTRONIC LOCATION AND ACCESS | |
| Uniform Resource Identifier | <a href="https://drive.google.com/file/d/1R4tRvyzVnDOBdYDtKCgOpfp_wSLQNZuU/view?usp=drivesdk">https://drive.google.com/file/d/1R4tRvyzVnDOBdYDtKCgOpfp_wSLQNZuU/view?usp=drivesdk</a> |
| Public note | Para ver el documento ingresa a Google con tu cuenta: @cicy.edu.mx |
| 942 ## - ADDED ENTRY ELEMENTS (KOHA) | |
| Source of classification or shelving scheme | Clasificación local |
| Koha item type | Documentos solicitados |
| Lost status | Source of classification or shelving scheme | Damaged status | Not for loan | Collection | Home library | Current library | Shelving location | Date acquired | Total checkouts | Full call number | Date last seen | Price effective from | Koha item type |
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| Clasificación local | Ref1 | CICY | CICY | Documento préstamo interbibliotecario | 25.06.2025 | B-18770 | 25.06.2025 | 25.06.2025 | Documentos solicitados |
