@article {5327, title = {Molecular diversity of Dscam and self-recognition.}, journal = {Advances in Experimental Medicine and Biology}, volume = {739}, year = {2012}, month = {2012}, pages = {262-75}, abstract = {

Cell recognition requires interactions through molecules located on cell surface. The insect homolog of Down syndrome cell adhesion molecule (Dscam) manifests huge molecular diversity in its extracellular domain. High-affinity Dscam-Dscam interactions only occur between isoforms that carry identical extracellular domains. Homophilic Dscam signaling can, thus, vary in strength depending on the compositions of Dscams present on the opposing cell surfaces. Dscam abundantly exists in the developing nervous system and governs arborization and proper elaboration of neurites. Notably, individual neurons may stochastically and dynamically express a small subset of Dscam isoforms such that any given neurite can be endowed with a unique repertoire of Dscams. This allows individual neurites to recognize their sister branches. Self-recognition leads to self-repulsion, ensuring divergent migration of sister processes. By contrast, weak homophilic Dscam interactions may promote fasciculation of neurites that express analogous, but not identical, Dscams. Differential Dscam binding may provide graded cell recognition that in turn governs complex neuronal morphogenesis.

}, keywords = {Animals, Cell Adhesion Molecules, Cell Communication, Drosophila Proteins, Gene Expression Regulation, Neurons, Protein Isoforms}, issn = {0065-2598}, doi = {10.1007/978-1-4614-1704-0_17}, author = {Shi, Lei and Lee, Tzumin} } @article {781, title = {Twin-spot MARCM to reveal the developmental origin and identity of neurons.}, journal = {Nature Neuroscience}, volume = {12}, year = {2009}, month = {2009 Jul}, pages = {947-53}, abstract = {

A comprehensive understanding of the brain requires the analysis of individual neurons. We used twin-spot mosaic analysis with repressible cell markers (twin-spot MARCM) to trace cell lineages at high resolution by independently labeling paired sister clones. We determined patterns of neurogenesis and the influences of lineage on neuron-type specification. Notably, neural progenitors were able to yield intermediate precursors that create one, two or more neurons. Furthermore, neurons acquired stereotyped projections according to their temporal position in various brain sublineages. Twin-spot MARCM also permitted birth dating of mutant clones, enabling us to detect a single temporal fate that required chinmo in a sublineage of six Drosophila central complex neurons. In sum, twin-spot MARCM can reveal the developmental origins of neurons and the mechanisms that underlie cell fate.

}, keywords = {Animals, Brain, Cell Lineage, Central Nervous System, Drosophila, Drosophila Proteins, Gene Knockout Techniques, Genetic Techniques, Genetically Modified, Mushroom Bodies, Nerve Tissue Proteins, Neurogenesis, Neurons, RNA Interference, Time Factors}, issn = {1546-1726}, doi = {10.1038/nn.2345}, author = {Yu, Hung-Hsiang and Chen, Chun-Hong and Shi, Lei and Huang, Yaling and Lee, Tzumin} } @article {793, title = {Specific Drosophila Dscam juxtamembrane variants control dendritic elaboration and axonal arborization.}, journal = {The Journal of Neuroscience: The Official Journal of the Society for Neuroscience}, volume = {27}, year = {2007}, month = {2007 Jun 20}, pages = {6723-8}, abstract = {

Drosophila Dscam isoforms are derived from two alternative transmembrane/juxtamembrane domains (TMs) in addition to thousands of ectodomain variants. Using a microRNA-based RNA interference technology, we selectively knocked down different subsets of Dscams containing either the exon 17.1- or exon 17.2-encoding TM. Eliminating Dscam[TM1] reduced Dscam expression but minimally affected postembryonic axonal morphogenesis. In contrast, depleting Dscam[TM2] blocked axon arborization. Further removal of Dscam[TM1] enhanced the loss-of-Dscam[TM2] axonal phenotypes. However, Dscam[TM1] primarily regulates dendritic development, as evidenced by the observations that removing Dscam[TM1] alone impeded elaboration of dendrites and that transgenic Dscam[TM1], but not Dscam[TM2], effectively rescued Dscam mutant dendritic phenotypes in mosaic organisms. These distinct Dscam functions can be attributed to the juxtamembrane regions of TMs that govern dendritic versus axonal targeting of Dscam as well. Together, we suggest that specific Drosophila Dscam juxtamembrane variants control dendritic elaboration and axonal arborization.

}, keywords = {Animals, Axons, Cell Adhesion Molecules, Dendrites, Drosophila, Drosophila Proteins, Genetic Variation, Genetically Modified, Membrane Proteins, Morphogenesis, Neural Cell Adhesion Molecules, Protein Isoforms}, issn = {1529-2401}, doi = {10.1523/JNEUROSCI.1517-07.2007}, author = {Shi, Lei and Yu, Hung-Hsiang and Yang, Jacob S and Lee, Tzumin} }