K Zarbalis, J Siegenthaler, Y Choe, SR May, A Peterson, SJ Pleasure (2007) Cortical dysplasia and skull defects in mice with a Foxc1 allele reveal the role of meningeal differentiation in regulating cortical development. PNAS, PNAS 104:14002-14007.

MF Paredes, G Li, O Berger, SC Baraban, SJ Pleasure (2006) SDF1 (CXCL12) regulates laminar position of Cajal-Retzius cells in normal and dysplastic brains. Journal of Neuroscience, 26:9404-9412. Chosen as featured article for the issue
This study establishes that the chemokine SDF1, produced by the meninges, is necessary for normal Cajal-Retzius cell positioning. These cells are located adjacent to the meninges during development and in turn control the migratory behavior of radially organized cortical neurons. We also show that in a rodent model of teratogenic cortical dysplasia with disorganization of Cajal-Retzius cells that this portion of the histologic defect is due to the loss of SDF1 signaling in the meninges and that SDF1 signaling is both necessary and sufficient to rescue this histologic defect.

C Zhao, C Avilés, RA Abel, CR Almli, P McQuillen, SJ Pleasure (2005) Hippocampal and visuospatial learning defects in mice with deletion of Frizzled9, a gene in the Williams syndrome deletion interval. Development 132:2917-2927.
This study examined the phenotype of mice with mutations in the Wnt receptor Frizzled9. This gene is contained within the deletion interval for Williams Syndrome. Williams Syndrome is a complex neurodevelopmental disorder with patients showing prominent visuospatial processing abnormalities, out of proportion to other cognitive deficits. The mutant mice demonstrated structural and functional hippocampal dysfunction both in the heterozygous (similar genotype as patients with Williams) and homozygous states. This indicates that loss of this Wnt receptor and the resulting hippocampal abnormalities are likely to be part of the clinical syndrome of Williams.

CJ Zhou, C Zhao, SJ Pleasure (2004) Wnt signaling mutants have decreased dentate granule cell production and radial glial scaffolding abnormalities. Journal of Neuroscience 24:121-126.
In this study we examined the phenotype of dentate gyrus abnormalities in the LRP6 mutants, these mice have widespread defects in Wnt signaling. We found that these mice had defects at multiple levels in producing dentate granule neurons, including specification of the neuroepithelium, establishing the radial glial scaffolding and precursor proliferation. I supervised every aspect of this work including the data acquisition, analysis and writing of the paper.

A Bagri, HJ Cheng, A Yaron, SJ Pleasure*, M Tessier-Lavigne* (2003) Stereotyped pruning of long hippocampal axon branches triggered by retraction inducers of the Semaphorin family. Cell 113:285-299.    *co-corresponding authors
In this papers we examined the consequences of loss of Semaphorin signaling on the development of hippocampal afferent and efferent projections. We showed in this work that semaphorins regulate the critically important process of axonal pruning during hippocampal development. Dr. Tessier-Lavigne and I contributed equally to the conception of the experiments described here as well as the interpretation of data and writing of the manuscript. This work is part of an ongoing collaborative initiative with Dr. Marc Tessier-Lavigne to characterize the basic mechanisms of axon guidance in the hippocampus.

A Bagri, T Gurney, X He, Y-R Zou, D Littman, M Tessier-Lavigne*, SJ Pleasure* (2002) The chemokine SDF-1 regulates migration of dentate granule neurons. Development 129:4249-4260. *co-corresponding authors
In this study we showed that the chemokine SDF1 is a direct chemoattractant for dentate granule neurons. Loss of signaling of this molecule leads to heterotopic granule neurons because of failed migration and also a defect in granule cell precursor proliferation. Dr. Tessier-Lavigne and I contributed equally to the conception of the experiments described here as well as the interpretation of data and writing of the manuscript.