Home > Funded Projects > The molecular mechanism of SNORD116 action and possible SNORD116 substitution strategies

The loss of two snoRNAs, SNORD115 and SNORD116, plays a central role in the development of Prader-Willi syndrome. However, the normal function of SNORD116 is still unclear, making it difficult to understand what goes wrong when SNORD116 is lost. Dr. Stamm’s group is exploring how SNORD116 influences other genes, and their preliminary studies indicate that SNORD116 regulates a number of other RNAs. Here, they will define the genes that SNORD116 targets, potentially establishing new therapeutic targets, and explore approaches to replace SNORD116 function.

ABSTRACT: The loss of two snoRNAs, SNORD115 and SNORD116 plays a central role in the development of Prader-Willi syndrome. The role of SNORD116 has been enigmatic, as it was not possible to determine its targets bioinformatically. We devised a new strategy to remove SNORD116 from cells and could thus compare cells with and without this RNA. We found that SNORD116 regulates the expression of about 500 RNAs, as well as the structure of about 50 RNAs. We will further validate these findings and test an oligonuclotide for its ability to substitute the loss of SNORD116.

Funded Year:

2016

Awarded to:

Stefan Stamm, PhD

Amount:

$70,000

Institution:

University of Kentucky

Researcher: