Cells use RNA to regulate their genes. Some smallRNAs can shut genes off, while others can fine-tune how much is produced from various genes. Plants, worms, and humans all use the same thing: the ability to chop up the small pieces of the RNA of invading Viruses, worms, and humans. It hasn't been clear exactly why some human cancers are caused by the genes for theidase, but it is of interest because of the fact that the genes for theidase appear to contribute to some human cancers.
In a new study published in the journal Nature Communications, Cold Spring Harbor Laboratory Professor Rob Martienssen and his team found an unexpected role for Dicer in mammals.
The stem cells of the mice became sick when they were removed. The chymosomes inside dividing cells couldn't align themselves for equal distribution to daughter cells. Many cells died as cell division slowed. When they removed Dicer from yeast cells, they had seen this before. They discovered that the mouse genome is similar to the one in yeast, suggesting that this is an ancient role for the enzyme.
The new function that we have identified for Dicer genome stability, independently of other well-known small RNA pathways, could be an explanation of why Dicer is an important factor in certain types of cancer.
BRD4 is a gene-activatingProtein that is normally used by Dicer. When BRD4 was intact, the research team found that the chromosomes were unstable. A small piece of BRD4 was removed to restore chromosome stability. BRD4 is often found in human cancers. The work suggests a new diagnostic and treatment strategy for cancers with compromised Dicer systems using BRD4-targeting.
More information: M. J. Gutbrod et al, Dicer promotes genome stability via the bromodomain transcriptional co-activator BRD4, Nature Communications (2022). DOI: 10.1038/s41467-022-28554-8 Journal information: Nature Communications Citation: Stabilizing chromosomes to tackle tumors (2022, March 17) retrieved 17 March 2022 from https://phys.org/news/2022-03-stabilizing-chromosomes-tackle-tumors.html This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only.
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