Mouse Fkbp8 activity is required to inhibit cell death and establish DV patterning in the posterior neural tube

Mouse Fkbp8 mutants specifically present with spinal cord abnormalities and spina bifida. The aim is to identify gene expression changes in the posterior embryonic tissue lacking the Fkbp8 gene, so as to understand genes or gene pathways important for normal spinal cord development. Keywords: Genetic modification Heterozygous Fkbp8 mutant mice were intercrossed to obtain embryos of all three genotypes. Posterior tissue (immediately after forelimb bud) was dissected from E9.5 embryos and RNA extracted. Three wildtype tissues and three mutant tissues were used for hybridization on commercially available CodeLink Mouse Whole Genome array.小鼠Fkbp8突变体仅表现出脊髓异常与脊柱裂（spina bifida）。本研究旨在鉴定缺失Fkbp8基因的胚胎后部组织中的基因表达变化，以阐明对正常脊髓发育至关重要的基因及基因通路。 关键词：基因修饰 通过互交杂合Fkbp8突变小鼠，获得携带三种基因型的胚胎。于胚胎发育第9.5天（E9.5）的胚胎中分离前肢芽紧邻区域的后部组织并提取RNA。选取3份野生型组织与3份突变型组织，在商用CodeLink小鼠全基因组表达芯片上完成杂交实验。