Imagine a cell like a concert hall and DNA as the sheet music. For the show to run smoothly, only the right notes should be played at the right time—this is gene expression. But if the orchestra hits the wrong notes, chaos follows: the cell forgets its role or behaves strangely.
Now, picture this happening in brain cells as they’re forming. One out-of-sync solo, and it could disrupt the entire performance, potentially contributing to conditions like autism.
In a major leap forward, researchers at the University of Geneva have discovered two proteins—MLF2 and RBM15—that play a key role in chromatin remodeling, the vital process that controls how genes are turned on or off.
When this process goes awry, it can lead to a range of diseases. The newly identified proteins act like fine-tuners of this genetic machinery and could become powerful drug targets. What’s more, therapies based on them may be less toxic than current options.
Scientists uncovered 60 new autism genes
To pinpoint these proteins, scientists turned to CRISPR-Cas9 gene-editing technology. After scanning more than 20,000 genes, MLF2 and RBM15 emerged as the standout candidates.
Now that MLF2 and RBM15 have been identified as key players in gene regulation, scientists are digging deeper. The next step is to find out whether targeting these proteins can actually destroy cancer cells or simply hold them back.
Looking further ahead, the ultimate goal is to uncover the most effective drug compounds that can restore balance to faulty chromatin remodeling, potentially offering safer and more precise treatments for diseases driven by genetic misfires.
Journal Reference:
- Schwaemmle, H., Soldati, H., Lykoskoufis, N.M.R. et al. CRISPR screen decodes SWI/SNF chromatin remodeling complex assembly. Nat Commun 16, 5011 (2025). DOI: 10.1038/s41467-025-60424-x
