A group of eleven zebrafish genes yielded R2 of 1 and a slope of 0.99, while a group of seven mouse liver genes yielded a R2 of 0.98 and a slope of 0.97, and seven mouse brain genes yielded a R2 of 0.95 and a slope of 0.87.
In order to elucidate how genes involved in neurite outgrowth and elongation interact to promote neuritogenesis in the Glud1 mouse brain, a gene network was constructed for these genes and their partners.
The final list included 57 human brain specific genes and 50 mouse brain specific genes.
In these gene groups, the entropy in most ectopic ranked tissue positions was above 0.7 and the ectopic expression index ranged from 1.1 and 1.5 for human and mouse brain specific genes respectively, to respectively 1.5 and 1.4 for spermatogenesis-related genes in human and mouse.
Notably, as in humans, the genes from the yellow module are also enriched in the early embryonic mouse brain whereas genes from the brown module are enriched in the late embryonic mouse brain (supplementary material Fig. S5C).
Surprisingly, the SDEG involved in the alternate pathway (C3a, C3b, Bfa, Bfb and Hf1) were significantly up-regulated in the mutant-infected mouse brain; these genes were not significantly affected during wild type-infection.
The virions expressing the desired genes of interest are directly delivered to the mouse brain to induce gene expression in Nestin, GFAP, or Cnp-expressing cells.
FAM5C was originally identified in the mouse brain as a gene that is induced by bone morphogenic protein and retinoic acid signaling [23].
It has not been previously reported that gliomas induced with the same genetic alterations in different regions of the mouse brain have distinct gene expression.
Although ABA data may extend from mouse brain tissue, all genes listed in Table 1 are orthologous to rat and human genes according to the Mouse Genome Informatics database (http://www.informatics.jax.org).org
