Key Points
- Scientists have discovered a new, crucial role for an ancient protein called Dicer.
- Dicer helps to prevent dangerous “collisions” between the processes of copying DNA and making RNA.
- These collisions can cause DNA damage, which can lead to cancer.
- Dicer works by “pausing” the RNA synthesis machinery to give DNA repair systems time to act.
Scientists have discovered a new and vital role for an ancient protein called Dicer, a molecule that both humans and yeast inherited from a common ancestor who lived 2 billion years ago. The new research, published in Molecular Cell, shows that Dicer acts as a crucial traffic cop, helping prevent dangerous “collisions” inside our cells that can lead to DNA damage and cancer.
The problem arises when two fundamental cellular processes—DNA replication and RNA transcription—occur simultaneously and overlap.
These “collisions” can create tangled structures called R-loops, which can break our DNA. “When T–R collisions occur, it’s like a broken zipper,” explains Professor Rob Martienssen of Cold Spring Harbor Laboratory.
Scientists already knew that an enzyme called RNase H helps to clean up these messes. But now, Martienssen’s team has found that Dicer is also essential. It works by temporarily “pausing” the RNA-making machinery, which gives the DNA repair process time to work. “Without Dicer, repair still occurs, but it causes mutations, cancer, and other issues,” Martienssen says.
This discovery changes our fundamental understanding of Dicer. “We’ve always thought of it as part of some sort of immune system, but Dicer clearly evolved from a transcription-replication origin,” he says. “That has profound implications for how we think about Dicer and understand fundamental processes of life itself.”
