التفاصيل البيبلوغرافية
| العنوان: |
SETDB1-like MET-2 promotes transcriptional silencing and development independently of its H3K9me-associated catalytic activity |
| المؤلفون: |
Colin E. Delaney, Stephen P. Methot, Veronique Kalck, Jan Seebacher, Daniel Hess, Susan M. Gasser, Jan Padeken |
| المصدر: |
Nature Structural and Molecular Biology |
| سنة النشر: |
2022 |
| مصطلحات موضوعية: |
Structural Biology, Molecular Biology |
| الوصف: |
Transcriptionally silenced heterochromatin bearing methylation of histone H3 on lysine 9 (H3K9me) is critical for maintaining organismal viability and tissue integrity. Here we show that in addition to ensuring H3K9me, MET-2, the Caenorhabditis elegans homolog of the SETDB1 histone methyltransferase, has a noncatalytic function that contributes to gene repression. Subnuclear foci of MET-2 coincide with H3K9me deposition, yet these foci also form when MET-2 is catalytically deficient and H3K9me is compromised. Whereas met-2 deletion triggers a loss of silencing and increased histone acetylation, foci of catalytically deficient MET-2 maintain silencing of a subset of genes, blocking acetylation on H3K9 and H3K27. In normal development, this noncatalytic MET-2 activity helps to maintain fertility. Under heat stress MET-2 foci disperse, coinciding with increased acetylation and transcriptional derepression. Our study suggests that the noncatalytic, focus-forming function of this SETDB1-like protein and its intrinsically disordered cofactor LIN-65 is physiologically relevant. |
| تدمد: |
1545-9993 |
| DOI: |
10.1038/s41594-021-00712-4 |
| URL الوصول: |
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::56639854f977f10a32e97805dcfb0a77 |
| Rights: |
OPEN |
| رقم الانضمام: |
edsair.doi.dedup.....56639854f977f10a32e97805dcfb0a77 |
| قاعدة البيانات: |
OpenAIRE |