Where Form 5495 Compensation 2017-2025

Hello, my name is DDS tinium, directed the Max Planck Institute for Research in Bad Nauheim, Germany. Today, in this third part, we're going to be talking about the phenomenon of genetic compensation in the context of a scary development in the zebrafish embryo. Historically, gene function in zebrafish has been studied initially through a full genetic approach, mainly utilizing the genome to introduce mutations randomly and then doing phenotypic screening. More recently, morpholino antisense oligonucleotides have been used to knockdown gene function, and just a few years ago, zinc finger nucleases as well as TALENs and CRISPR-Cas9 technology mutations have been introduced in specific genes to study not only genes that were previously studied using morpholinos, but also other genes. The studies that I'll be telling you about today are essentially inspired by the fact that when looking at specific genes that have been studied using morpholinos as well as reverse genetic techniques, it became apparent that in many cases, the phenotypes induced by mutations were much milder than those induced by the morpholino technology. Just to give you a little background, morpholinos are modifying all egos, highly stable, they bind RNA, and they are used to either block translation or splicing. The question then is why mutant phenotypes are much milder than morpholino-induced phenotypes. Mutant phenotypes are often referred to as knockouts, while antisense knockdowns are referred to as morpholinos. Now, let's understand some history of the antisense approach. More than thirty years ago, people working in developmental biology started using antisense RNA in the context of frog embryos and fly embryos. However, this approach was fairly short-lived, probably because people were concerned about off-target effects, and they moved on to overexpressing wild-type or dominant-negative versions of genes or proteins. Despite the imperfections of these reagents, they have...