Regulated vnd expression is required for both neural and glial specification in Drosophila
dc.contributor.author | Mellerick, Dervla M. | en_US |
dc.contributor.author | Modica, Victoria | en_US |
dc.date.accessioned | 2006-04-19T13:36:24Z | |
dc.date.available | 2006-04-19T13:36:24Z | |
dc.date.issued | 2002-02-05 | en_US |
dc.identifier.citation | Mellerick, Dervla M.; Modica, Victoria (2002)."Regulated vnd expression is required for both neural and glial specification in Drosophila ." Journal of Neurobiology 50(2): 118-136. <http://hdl.handle.net/2027.42/34482> | en_US |
dc.identifier.issn | 0022-3034 | en_US |
dc.identifier.issn | 1097-4695 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/34482 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=11793359&dopt=citation | en_US |
dc.description.abstract | The Drosophila embryonic CNS arises from the neuroectoderm, which is divided along the dorsal-ventral axis into two halves by specialized mesectodermal cells at the ventral midline. The neuroectoderm is in turn divided into three longitudinal stripes—ventral, intermediate, and lateral. The ventral nervous system defective, or vnd, homeobox gene is expressed from cellularization throughout early neural development in ventral neuroectodermal cells, neuroblasts, and ganglion mother cells, and later in an unrelated pattern in neurons. Here, in the context of the dorsal-ventral location of precursor cells, we reassess the vnd loss- and gain-of-function CNS phenotypes using cell specific markers. We find that over expression of vnd causes significantly more profound effects on CNS cell specification than vnd loss. The CNS defects seen in vnd mutants are partly caused by loss of progeny of ventral neuroblasts—the commissures are fused and the longitudinal connectives are aberrantly positioned close to the ventral midline. The commissural vnd phenotype is associated with defects in cells that arise from the mesectoderm, where the VUM neurons have pathfinding defects, the MP1 neurons are mis-specified, and the midline glia are reduced in number. vnd over expression results in the mis-specification of progeny arising from all regions of the neuroectoderm, including the ventral neuroblasts that normally express the gene. The CNS of embryos that over express vnd is highly disrupted, with weak longitudinal connectives that are placed too far from the ventral midline and severely reduced commissural formation. The commissural defects seen in vnd gain-of-function mutants correlate with midline glial defects, whereas the mislocalization of interneurons coincides with longitudinal glial mis-specification. Thus, Drosophila neural and glial specification requires that vnd expression by tightly regulated. © 2002 Wiley Periodicals, Inc. J Neurobiol 50: 118–136, 2002; DOI 10.1002/neu.10022 | en_US |
dc.format.extent | 5078190 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Wiley Periodicals, Inc. | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Neuroscience, Neurology and Psychiatry | en_US |
dc.title | Regulated vnd expression is required for both neural and glial specification in Drosophila | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbsecondlevel | Psychology | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Social Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Pathology, University of Michigan Medical Center, Ann Arbor, Michigan 48109 ; Department of Pathology, University of Michigan Medical Center, Ann Arbor, Michigan 48109 | en_US |
dc.contributor.affiliationum | Department of Pathology, University of Michigan Medical Center, Ann Arbor, Michigan 48109 | en_US |
dc.identifier.pmid | 11793359 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/34482/1/10022_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/neu.10022 | en_US |
dc.identifier.source | Journal of Neurobiology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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