ribosomal protein gene knockdown causes developmental defects in zebrafish核糖体蛋白基因击倒导致斑马鱼发育缺陷.pdfVIP

Ribosomal Protein Gene Knockdown Causes Developmental Defects in Zebrafish 1 1 1 1 1 2 1 Tamayo Uechi , Yukari Nakajima , Akihiro Nakao , Hidetsugu Torihara , Anirban Chakraborty , Kunio Inoue , Naoya Kenmochi * 1 Frontier Science Research Center, University of Miyazaki, Miyazaki, Japan, 2 Department of Biology, Graduate School of Science and Technology, Kobe University, Kobe, Japan The ribosomal proteins (RPs) form the majority of cellular proteins and are mandatory for cellular growth. RP genes have been linked, either directly or indirectly, to various diseases in humans. Mutations in RP genes are also associated with tissue- specific phenotypes, suggesting a possible role in organ development during early embryogenesis. However, it is not yet known how mutations in a particular RP gene result in specific cellular changes, or how RP genes might contribute to human diseases. The development of animal models with defects in RP genes will be essential for studying these questions. In this study, we knocked down 21 RP genes in zebrafish by using morpholino antisense oligos to inhibit their translation. Of these 21, knockdown of 19 RPs resulted in the development of morphants with obvious deformities. Although mutations in RP genes, like other housekeeping genes, would be expected to result in nonspecific developmental defects with widespread phenotypes, we found that knockdown of some RP genes resulted in phenotypes specific to each gene, with varying degrees of abnormality in the brain, body trunk, eyes, and ears at about 25 hours post fertilization. We focused further on the organogenesis of the brain. Each knocked-down gene that affected the morphogenesis of the brain produced a different patte