deletion of snap-23 results in pre-implantation embryonic lethality in mice删除snap-23导致胚胎植入前胚胎小鼠的杀伤力.pdfVIP

Deletion of SNAP-23 Results in Pre-Implantation Embryonic Lethality in Mice 1,2,3 5 1 4 2 Young Ho Suh , Aki Yoshimoto-Furusawa , Karis A. Weih , Lino Tessarollo , Katherine W. Roche , 5 1 Susan Mackem , Paul A. Roche * 1 Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America, 2 Receptor Biology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America, 3 Neuroscience Graduate Program, Department of Pharmacology, Ajou University School of Medicine, Suwon, South Korea, 4 Mouse Cancer Genetics Program, Center for Cancer Research (CCR), NCI- Frederick, National Institutes of Health, Frederick, Maryland, United States of America, 5 Cancer and Developmental Biology Laboratory, Center for Cancer Research (CCR), NCI-Frederick, National Institutes of Health, Frederick, Maryland, United States of America Abstract SNARE-mediated membrane fusion is a pivotal event for a wide-variety of biological processes. SNAP-25, a neuron-specific SNARE protein, has been well-characterized and mouse embryos lacking Snap25 are viable. However, the phenotype of mice lacking SNAP-23, the ubiquitously expressed SNAP-25 homolog, remains unknown. To reveal the importance of SNAP-23 function in mouse development, we generated Snap23-null mice by homologous recombination. We were unable to obtain newborn SNAP-23-deficient mice, and analysis of pre-implantation embryos from Snap23D/wt matings revealed that Snap23- null blastocysts were dying prior to implantation at embryonic day E3.5. Thus these data reveal a critical role for SNAP-23 during embryo