Sgf29, a component of the SAGA transcriptional coactivator complex, is involved in multiple biological functions. It participates in histone post-translational modifications as part of the Ada2/Ada3/Gcn5/Sgf29 histone acetyltransferase module, where Gcn5, a histone acetyltransferase, catalyzes histone H3 acetylation in this module context [2]. Sgf29 also binds histone H3K4me2/3, which is essential for SAGA complex recruitment and histone H3 acetylation [5]. It has significance in gene regulation, and its dysregulation may be related to various diseases.

In acute myeloid leukemia (AML) models, Sgf29 deletion impaired leukemogenesis. It was identified as a regulator of the transcription of AML oncogenes, such as the key leukemia stem cell-associated gene MEIS1 [4]. In hepatocarcinogenesis, elevated SGF29 expression contributes to the oncogenic potential of c-Myc, and the Sry-SGF29 pathway may be implicated in the male-specific acquisition of human HCCs [3]. In human mesenchymal progenitor cells (hMPCs) and fibroblasts, during cellular senescence, SGF29 forms liquid-like nuclear condensates. The Arg 207 within its intrinsically disordered region is key for phase separation. These condensates are important for establishing chromatin location, recruiting transcriptional factors, and initiating the expression of senescence-associated genes like CDKN1A [1].

In conclusion, Sgf29 plays essential roles in histone modification, gene regulation, and is involved in processes like cellular senescence, leukemogenesis, and hepatocarcinogenesis. Studies using loss-of-function models in these disease areas have revealed its significance, providing insights into potential therapeutic targets and disease mechanisms related to these conditions.