Bcl7a, a subunit of the SWI/SNF chromatin remodeling complexes, plays crucial roles in multiple biological processes. It is involved in regulating Notch/Wnt pathway signaling and mitochondrial bioenergetics during neural progenitor cell (NPC) differentiation. In plants, Bcl7a and Bcl7b potentiate SWI/SNF-complex-mediated chromatin accessibility to regulate gene expression and vegetative phase transition [1,5].

In conditional Bcl7a knockout mice, Bcl7a expression in NPCs and postmitotic neurons was found to be required for neuronal plasticity and support behavioral and cognitive performance. This indicates its importance in the cell-intrinsic transcriptional processes connecting metabolism, neuronal morphogenesis, and cognitive flexibility [1]. In acute myeloid leukemia (AML), restoring Bcl7a expression exerts tumor suppressor activity, as its downregulation in AML due to promoter hypermethylation is associated with increased malignancy and drug resistance [2,3]. In glioma, Bcl7a is a new tumor suppressor gene and can be used as a biomarker for independent prognosis and to evaluate response to chemotherapy [4].

In conclusion, Bcl7a is essential for regulating important biological processes, such as neural progenitor differentiation and plant development. Its knockout or conditional knockout mouse models have revealed its significance in neurodegenerative-related cognitive functions and in diseases like AML and glioma. These findings contribute to a better understanding of the underlying mechanisms and may offer potential therapeutic targets for these diseases.