| 2011 |
Crystal structures of the tandem Tudor domains of S. cerevisiae and human SGF29 bound to H3K4me2 and H3K4me3 peptides revealed that the two Tudor domains pack face-to-face, with one pocket accommodating the H3A1 residue and the other the methylated K4 residue. The limited cleft length between the two pockets confers selectivity for H3K4me2/3. In vitro and in vivo functional assays demonstrated that H3K4me2/3 recognition by SGF29 is required for SAGA complex recruitment to target gene loci and consequent histone H3 acetylation. |
Crystal structure (X-ray crystallography), peptide binding assays, in vivo ChIP and histone acetylation assays, mutagenesis of binding pockets |
The EMBO journal |
High |
21685874
|
| 2010 |
The tandem Tudor domain at the C-terminus of S. cerevisiae Sgf29 was successfully crystallized and diffracted to 1.92 Å resolution, confirming the domain adopts a distinct structural fold amenable to high-resolution analysis. |
X-ray crystallography (preliminary crystallographic analysis) |
Acta crystallographica. Section F, Structural biology and crystallization communications |
Medium |
20693663
|
| 2007 |
Rat SGF29 directly interacted with rADA3 (direct interaction) and co-immunoprecipitated with rGCN5 and rSPT3, establishing it as a component of the TFTC/STAGA complexes. SGF29 was recruited to c-Myc target gene promoters together with c-Myc and activated c-Myc target gene expression. Knockdown of rSGF29 suppressed c-Myc target gene expression and inhibited anchorage-independent growth, tumorigenicity, and lung metastasis. |
Co-immunoprecipitation, ChIP, gene expression assays, siRNA knockdown, in vivo tumor xenograft assay |
Oncogene |
Medium |
17334388
|
| 2013 |
Human SGF29 is a subunit of both the SAGA and ATAC histone acetyltransferase/co-activator complexes. SGF29 knockdown impaired transcription of ER stress genes GRP78 and CHOP, and reduced H3K14 acetylation at these loci. Additionally, SGF29 was required for maintenance of H3K4me3 at these promoters prior to ER stress; reduced H3K4me3 in SGF29-depleted cells correlated with decreased association of ASH2L (a core SET1/MLL complex component) at these gene loci, indicating a role for SGF29 in coordinating both H3K4me3 maintenance and H3K14 acetylation. |
siRNA knockdown, ChIP, quantitative RT-PCR, mass spectrometry-based complex identification |
PloS one |
Medium |
23894581
|
| 2013 |
In S. cerevisiae, domain analysis identified two minimal boundary-forming regions in Sgf29: the N-terminal region (aa 1–12) and the Tudor domain-containing C-terminal region (aa 110–255). Critically, the boundary formation activity of these minimal regions was shown to be independent of Gcn5 acetyltransferase activity, and in vivo analysis showed Sgf29 and Gcn5 perform distinct functions at native telomere boundary regions. |
Yeast genetic boundary assay, domain deletion/truncation analysis, in vivo telomere boundary assay |
Journal of biochemistry |
Medium |
24307402
|
| 2023 |
SGF29 forms liquid-like nuclear condensates during cellular senescence in human mesenchymal progenitor cells and fibroblasts via phase separation. Arg207 within the intrinsically disordered region is the key residue for condensate formation. Both condensate formation and H3K4me3 binding are required for SGF29 to establish its chromatin localization, recruit transcription factors and co-activators to specific genomic loci, and activate senescence-associated genes including CDKN1A. Condensate formation alone is not sufficient for H3K4me3 binding or transactivation. |
Mutagenesis (R207 mutation), live-cell imaging of phase separation, ChIP-seq, ATAC-seq, RNA-seq, co-activator recruitment assays |
Cell discovery |
Medium |
37935676
|
| 2024 |
CRISPR-Cas9 domain-focused screen identified SGF29 as required for transcription of AML oncogenes including MEIS1. SGF29 deletion impaired leukemogenesis across multiple AML subtype models, establishing the SGF29 Tudor domain (H3K4me3 reader function) as a nononcogenic dependency in AML. |
CRISPR-Cas9 domain-focused library screen, CRISPR droplet sequencing, in vivo leukemia models |
Blood |
Medium |
38048593
|
| 2026 |
In mouse ESCs, Sgf29 knockout reduced H3K9ac and chromatin accessibility at promoters and enhancers of pluripotency genes, triggering differentiation. Sgf29 was shown to interact with Oct4 and Nanog (but not Sox2) to co-regulate pluripotency gene expression. Sgf29 KO reduced Oct4 binding to Nanog and Klf4 loci. Sgf29 knockdown in pre-implantation embryos reduced blastocyst rate and decreased H3K9ac, with aberrant Oct4 and Nanog expression. |
Knockout/knockdown in mESCs, co-immunoprecipitation (Sgf29 with Oct4/Nanog), ChIP-seq for H3K9ac and transcription factor binding, ATAC-seq, pre-implantation embryo assays |
Science China. Life sciences |
Medium |
41843375
|
| 2024 |
A high-throughput imaging-based CRISPR screen (TAILS) identified SGF29 as a promoter of the Alternative Lengthening of Telomeres (ALT) pathway, placing SGF29 functionally in telomere maintenance via recombination. |
High-throughput CRISPR screen with native FISH-based optical readout (TAILS) |
bioRxivpreprint |
Low |
bio_10.1101_2024.11.15.623791
|