Current evidence suggests that most Prader-Willi syndrome (PWS) traits result from loss of paternally inherited SNORD116 gene group. SNORD116 belong to a class of small nucleolar RNAs (snoRNAs), which are involved in modification of other RNA species. snoRNAs act as guides to define sites of target RNA modification by partner enzymes. Typically, a snoRNA would recognize its target by sequence complementarity. However, a number of snoRNAs including SNORD116 group do not appear to display any obvious sequence complementarity to typical snoRNA targets, indicating that they might influence other targets including mRNA to fine-tune protein expression in distinct cell types. Until recently, identification of RNA-RNA interactions was hampered by lack of relevant experimental techniques. Here, we propose to use a newly developed methodology that allows unbiased interrogation of cellular RNA-RNA interactions to uncover RNA targets of SNORD116, shining light on molecular mechanisms underlying Prader-Willi syndrome. We envision that identifying SNORD116 targets will also help to define new downstream drug targets and cause a shift in the focus of PWS therapeutic approaches

Funded Year:


Awarded to:

Tomaz Bratkovic, PhD




University of Ljubljana, Slovenia