Regulated <i>vnd</i> expression is required for both neural and glial specification in <i>Drosophila</i>

Wiley - Tập 50 Số 2 - Trang 118-136 - 2002
Dervla M. Mellerick1, Victoria Modica1
1Department of Pathology, University of Michigan Medical Center, Ann Arbor, Michigan, 48109

Tóm tắt

AbstractThe 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

Từ khóa


Tài liệu tham khảo

Arendt D, 1999, Comparison of early nerve cord development in insects and vertebrates, Development, 126, 2309, 10.1242/dev.126.11.2309

10.1038/260054a0

10.1242/dev.127.2.237

10.1242/dev.120.7.1895

Bossing T, 1996, The embryonic central nervous system lineages of Drosophila melanogaster. I Neuroblast lineages derived from the ventral half of the neuroectoderm, Dev Biol, 17, 941

10.1242/dev.118.2.401

10.1016/S0092-8674(00)80853-3

10.1038/19315

10.1016/0925-4773(95)00454-8

Buescher M, 1997, Mutations in lottchen cause cell fate transformations in both neuroblast and glioblast lineages in the Drosophila embryonic central nervous system, Development, 124, 673, 10.1242/dev.124.3.673

10.1007/BF02740668

10.1007/978-3-662-02454-6

10.1101/gad.12.22.3613

10.1126/science.8372355

10.1016/S0959-4388(99)00049-5

10.1101/gad.12.5.607

10.1016/S0925-4773(96)00583-7

10.1242/dev.116.4.855

10.1126/science.2892267

10.1038/333376a0

10.1002/j.1460-2075.1987.tb04817.x

10.1016/0092-8674(87)90037-7

10.1016/S0092-8674(01)00290-2

10.1126/science.6474176

10.1016/0092-8674(91)90571-F

10.1242/dev.121.2.317

10.1242/dev.124.17.3253

Higashijima S, 1996, eagle a member of the steroid receptor gene superfamily is expressed in a subset of neuroblasts and regulates the fate of their putative progeny in the Drosophila CNS, Development, 122, 527, 10.1242/dev.122.2.527

10.1038/377627a0

10.1016/S0896-6273(00)81169-1

Hummel T, 1999, Commissure formation in the embryonic CNS of Drosophila, Development, 126, 771, 10.1242/dev.126.4.771

Isshiki T, 1997, The role of the msh homeobox gene during Drosophila neurogenesis: implication for the dorsoventral specification of the neuroectoderm, Development, 124, 3099, 10.1242/dev.124.16.3099

10.1016/S0301-0082(00)00016-2

10.1016/0896-6273(90)90036-F

10.1002/j.1460-2075.1995.tb07355.x

10.1101/gad.7.2.229

10.1016/S0959-4388(99)00053-7

10.1242/dev.128.2.207

10.1016/0092-8674(91)90509-W

Landgraf M, 1997, The origin location and projections of the embryonic abdominal motorneurons of Drosophila, J Neurosci, 17, 9642, 10.1523/JNEUROSCI.17-24-09642.1997

Lee CM, 1999, The CNS midline cells and spitz class genes are required for proper patterning of Drosophila ventral neuroectoderm, Int J Dev Biol, 43, 305

10.1101/gad.14.2.147

Lundgren SE, 1995, Control of neuronal pathway selection by the Drosophila LIM homeodomain gene apterous, Development, 121, 1769, 10.1242/dev.121.6.1769

10.1101/gad.12.22.3603

10.1016/0896-6273(92)90234-5

10.1006/dbio.1995.1283

Menne TV, 1997, CNS midline cells in Drosophila induce the differentiation of lateral neural cells, Development, 124, 4949, 10.1242/dev.124.24.4949

Mlodzik M, 1990, Isolation and expression of scabrous a gene regulating neurogenesis in Drosophila, Genes Dev, 4, 1848, 10.1101/gad.4.11.1848

Patel NH, 1994, 446

10.1101/gad.3.6.890

10.1016/0092-8674(87)90706-9

10.1016/S0896-6273(00)00143-4

Schmid A, 1999, Clonal analysis of Drosophila embryonic neuroblasts: neural cell types axon projections and muscle targets, Development, 126, 4653, 10.1242/dev.126.21.4653

10.1002/(SICI)1521-1878(199911)21:11<922::AID-BIES4>3.0.CO;2-T

Skeath JB, 1994, The ventral nervous system defective gene controls proneural gene expression at two distinct steps during neuroblast formation in Drosophila, Development, 120, 1517, 10.1242/dev.120.6.1517

10.1038/376427a0

10.1242/dev.121.10.3187

10.1242/dev.121.11.3489

1986 IRL Press Oxford AC Spradling DB Roberts P‐element mediated transformation in Drosophila: A Practical Approach 175 197

Sussel L, 1999, Loss of Nkx21 homeobox gene function results in a ventral to dorsal molecular respecification within the basal telencephalon: evidence for a transformation of the pallidum into the striatum, Development, 126, 3359, 10.1242/dev.126.15.3359

10.1038/16275

10.1016/S0896-6273(00)81241-6

10.1016/0092-8674(93)90643-5

10.1242/dev.125.9.1599

10.1101/gad.12.22.3591

10.1016/0896-6273(95)90314-3

10.1101/gad.8.8.981

10.1101/gad.11.11.1396