Dual binding patterns of MBD proteins in mammals and in C. elegans. In mammals (left), previous studies show that most MBD3 binding sites overlap with MBD2 and the Nucleosome Remodeling and Deacetylase (NuRD) complex, while MBD2 also independently occupies additional regions enriched with DNA methylation (5-methylcytosine, 5mC). In Caenorhabditis elegans (C. elegans) (right), which lacks DNA methylation, MBD-2 (Cel-MBD-2) displays a dual binding pattern as in mammalian MBD2, despite lacking a methyl-binding domain. This model illustrates how MBD-2 can be guided by different epigenetic signals when DNA methylation is absent. Credit: Nature Communications (2026). DOI: 10.1038/s41467-026-68592-0
How do cells keep their genes under control when a key regulatory system disappears during evolution? Scientists at HKU School of Biological Sciences have found an answer by studying a microscopic soil-living roundworm. They discovered that cells can switch to an alternative epigenetic “backup” mechanism to manage gene activity when the usual system is missing. This hidden safety net has been conserved through evolution, showing how flexible and resilient life can be.
當演化過程中關鍵的基因調控系統消失，細胞如何維持運作？港大生物科學學院的科學家透過研究一種活於土壤的微型線蟲找到了答案。他們發現，當常見的表觀遺傳機制缺失時，細胞能啟動另一套替代機制來管理基因活性。這個隱藏的安全網在演化中被保留下來，展現生命的高度靈活與韌性。
Full Stories: https://tinyurl.com/4xcym894 (In English)
詳細內容: https://tinyurl.com/5y7evpjt (中文)