@article {6952,
	title = {Cell-type-based model explaining coexpression patterns of genes in the brain.},
	journal = {Proceedings of the National Academy of Sciences of the United States of America},
	volume = {111},
	year = {2014},
	month = {2014 Apr 8},
	pages = {5397-402},
	abstract = {<p>Spatial patterns of gene expression in the vertebrate brain are not independent, as pairs of genes can exhibit complex patterns of coexpression. Two genes may be similarly expressed in one region, but differentially expressed in other regions. These correlations have been studied quantitatively, particularly for the Allen Atlas of the adult mouse brain, but their biological meaning remains obscure. We propose a simple model of the coexpression patterns in terms of spatial distributions of underlying cell types and establish its plausibility using independently measured cell-type-specific transcriptomes. The model allows us to predict the spatial distribution of cell types in the mouse brain.</p>
},
	issn = {1091-6490},
	doi = {10.1073/pnas.1312098111},
	author = {Grange, Pascal and Bohland, Jason W and Okaty, Benjamin W and Sugino, Ken and Bokil, Hemant and Nelson, Sacha B and Ng, Lydia and Hawrylycz, Michael and Mitra, Partha P}
}
@article {45638,
	title = {Cell-type-specific repression by methyl-CpG-binding protein 2 is biased toward long genes.},
	journal = {Journal of Neuroscience},
	volume = {34},
	year = {2014},
	month = {2014 Sep 17},
	pages = {12877-83},
	abstract = {<p>Mutations in methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome and related autism spectrum disorders (Amir et al., 1999). MeCP2 is believed to be required for proper regulation of brain gene expression, but prior microarray studies in Mecp2 knock-out mice using brain tissue homogenates have revealed only subtle changes in gene expression (Tudor et al., 2002; Nuber et al., 2005; Jordan et al., 2007; Chahrour et al., 2008). Here, by profiling discrete subtypes of neurons we uncovered more dramatic effects of MeCP2 on gene expression, overcoming the "dilution problem" associated with assaying homogenates of complex tissues. The results reveal misregulation of genes involved in neuronal connectivity and communication. Importantly, genes upregulated following loss of MeCP2 are biased toward longer genes but this is not true for downregulated genes, suggesting MeCP2 may selectively repress long genes. Because genes involved in neuronal connectivity and communication, such as cell adhesion and cell-cell signaling genes, are enriched among longer genes, their misregulation following loss of MeCP2 suggests a possible etiology for altered circuit function in Rett syndrome.</p>
},
	issn = {1529-2401},
	doi = {10.1523/JNEUROSCI.2674-14.2014},
	author = {Sugino, Ken and Hempel, Chris M and Okaty, Benjamin W and Arnson, Hannah A and Kato, Saori and Dani, Vardhan S and Nelson, Sacha B}
}
