a point mutation in translation initiation factor eif2b leads to function- and time-specific changes in brain gene expression点突变在翻译起始因子eif2b导致功能和有时限的脑基因表达的变化.pdfVIP

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a point mutation in translation initiation factor eif2b leads to function- and time-specific changes in brain gene expression点突变在翻译起始因子eif2b导致功能和有时限的脑基因表达的变化.pdf

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a point mutation in translation initiation factor eif2b leads to function- and time-specific changes in brain gene expression点突变在翻译起始因子eif2b导致功能和有时限的脑基因表达的变化

A Point Mutation in Translation Initiation Factor eIF2B Leads to Function- and Time-Specific Changes in Brain Gene Expression 1 2¤ 1 2 1,3 Liraz Marom , Igor Ulitsky , Yuval Cabilly , Ron Shamir , Orna Elroy-Stein * 1 Department of Cell Research and Immunology, George S. Wise Faculty of Life Science, Tel Aviv University, Tel Aviv, Israel, 2 Blavatnik School of Computer Science, Tel Aviv University, Tel Aviv, Israel, 3 Interdisciplinary School of Neuroscience, Tel Aviv University, Tel Aviv, Israel Abstract Background: Mutations in eukaryotic translation initiation factor 2B (eIF2B) cause Childhood Ataxia with CNS Hypomyelination (CACH), also known as Vanishing White Matter disease (VWM), which is associated with a clinical pathology of brain myelin loss upon physiological stress. eIF2B is the guanine nucleotide exchange factor (GEF) of eIF2, which delivers the initiator tRNAMet to the ribosome. We recently reported that a R132H mutation in the catalytic subunit of this GEF, causing a 20% reduction in its activity, leads under normal conditions to delayed brain development in a mouse model for CACH/VWM. To further explore the effect of the mutation on global gene expression in the brain, we conducted a wide-scale transcriptome analysis of the first three critical postnatal weeks. Methodology/Principal Findings: Genome-wide mRNA expression of wild-type and mutant mice was profiled at postnatal (P) days 1, 18 and 21 to reflect the early proliferative stage prior to white matter establishment (P1) and the peak of oligodendrocye differentiation and myelin synthesis (P18 and P21). At each developmental stage, between 441 and 818 genes were