Corrigendum to “Slit2 is necessary for optic axon organization in the zebrafish ventral midline” [Cells Dev. 166 (2021 Jun) 203677. doi:10.1016/j.cdev.2021.203677]

Ventral midline cells in the neural tube have distinct properties at different rostrocaudal levels, apparently in response to differential signalling by axial mesoderm. Floor plate cells are induced by sonic hedgehog (SHH) secreted from the notochord whereas ventral midline cells of the rostral diencephalon (RDVM cells) appear to be induced by the dual actions of SHH and bone morphogenetic protein 7 (BMP7) from prechordal mesoderm. We have examined the cellular and molecular events that govern the program of differentiation of RDVM cells under the influence of the axial mesoderm. By fate mapping, we show that prospective RDVM cells migrate rostrally within the neural plate, passing over rostral notochord before establishing register with prechordal mesoderm at stage 7. Despite the co-expression of SHH and BMP7 by rostral notochord, prospective RDVM cells appear to be specified initially as caudal ventral midline neurectodermal cells and to acquire RDVM properties only at stage 7. We provide evidence that the signalling properties of axial mesoderm over this period are regulated by the BMP antagonist, chordin. Chordin is expressed throughout the axial mesoderm as it extends, but is downregulated in prechordal mesoderm coincident with the onset of RDVM cell differentiation. Addition of chordin to conjugate explant cultures of prechordal mesoderm and neural tissue prevents the rostralization of ventral midline cells by prechordal mesoderm. Chordin may thus act to refine the patterning of the ventral midline along the rostrocaudal axis.

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Ventral midline cells are required for the local control of commissural axon guidance in the mouse spinal cord

Development ◽

10.1242/dev.126.16.3649 ◽

1999 ◽

Vol 126 (16) ◽

pp. 3649-3659

Author(s):

M.P. Matise ◽

M. Lustig ◽

T. Sakurai ◽

M. Grumet ◽

A.L. Joyner

Keyword(s):

Spinal Cord ◽

Critical Role ◽

Floor Plate ◽

Posterior Commissure ◽

Ventral Midline ◽

Mouse Spinal Cord ◽

Commissural Axons ◽

Midline Cells

Specialized cells at the midline of the central nervous system have been implicated in controlling axon projections in both invertebrates and vertebrates. To address the requirement for ventral midline cells in providing cues to commissural axons in mice, we have analyzed Gli2 mouse mutants, which lack specifically the floor plate and immediately adjacent interneurons. We show that a Dbx1 enhancer drives tau-lacZ expression in a subpopulation of commissural axons and, using a reporter line generated from this construct, as well as DiI tracing, we find that commissural axons projected to the ventral midline in Gli2(−/−) embryos. Netrin1 mRNA expression was detected in Gli2(−/−) embryos and, although much weaker than in wild-type embryos, was found in a dorsally decreasing gradient. This result demonstrates that while the floor plate can serve as a source of long-range cues for C-axons in vitro, it is not required in vivo for the guidance of commissural axons to the ventral midline in the mouse spinal cord. After reaching the ventral midline, most commissural axons remained clustered in Gli2(−/−) embryos, although some were able to extend longitudinally. Interestingly, some of the longitudinally projecting axons in Gli2(−/−) embryos extended caudally and others rostrally at the ventral midline, in contrast to normal embryos in which virtually all commissural axons turn rostrally after crossing the midline. This finding indicates a critical role for ventral midline cells in regulating the rostral polarity choice made by commissural axons after they cross the midline. In addition, we provide evidence that interactions between commissural axons and floor plate cells are required to modulate the localization of Nr-CAM and TAG-1 proteins on axons at the midline. Finally, we show that the floor plate is not required for the early trajectory of motoneurons or axons of the posterior commissure, whose projections are directed away from the ventral midline in both WT and Gli2(−/−) embryos, although they are less well organized in Gli2(−/−)mutants.

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Determination of Neuroepithelial Cell Fate: Induction of the Oligodendrocyte Lineage by Ventral Midline Cells and Sonic Hedgehog

Developmental Biology ◽

10.1006/dbio.1996.0142 ◽

1996 ◽

Vol 177 (1) ◽

pp. 30-42 ◽

Cited By ~ 167

Author(s):

Nigel P. Pringle ◽

Wei-Ping Yu ◽

Sarah Guthrie ◽

Henk Roelink ◽

Andrew Lumsden ◽

...

Keyword(s):

Cell Fate ◽

Sonic Hedgehog ◽

Neuroepithelial Cell ◽

Ventral Midline ◽

Midline Cells

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EGFR signaling is required for the differentiation and maintenance of neural progenitors along the dorsal midline of the Drosophila embryonic head

Development ◽

10.1242/dev.125.17.3417 ◽

1998 ◽

Vol 125 (17) ◽

pp. 3417-3426 ◽

Cited By ~ 3

Author(s):

K. Dumstrei ◽

C. Nassif ◽

G. Abboud ◽

A. Aryai ◽

...

Keyword(s):

Optic Lobe ◽

Apoptotic Cell ◽

Growth Factor Receptor ◽

Loss Of Function ◽

Egfr Signaling ◽

Stomatogastric Nervous System ◽

Ventral Midline ◽

Ras Pathway ◽

Midline Cells ◽

Head Midline

EGFR signaling has been shown in recent years to be involved in the determination, differentiation and maintenance of neural and epidermal cells of the ventral midline (mesectoderm and ventromedial ectoderm). Localized activation of the TGFalpha homolog Spitz (Spi) in the mesectoderm is achieved by the products of the genes rhomboid and Star. Spi binds to its receptor, the Drosophila epidermal growth factor receptor homolog (Egfr), and triggers the Ras pathway which is needed for the survival and differentiation of ventral midline cells. The results reported here indicate that EGFR signaling is also required in a narrow medial domain of the head ectoderm (called ‘head midline’ in the following) that includes the anlagen of the medial brain, the visual system (optic lobe, larval eye) and the stomatogastric nervous system (SNS). We document that genes involved in EGFR signaling are expressed in the head midline. Loss of EGFR signaling results in an almost total absence of optic lobe and larval eye, as well as severe reduction of SNS and medial brain. The cellular mechanism by which this phenotype arises is a failure of neurectodermal cells to differentiate combined with apoptotic cell death. Overactivity of EGFR signaling, as achieved by heat-shock-driven activation of a wild-type rhomboid (rho) construct, or by loss of function of argos (aos) or yan, results in an hyperplasia and deformity of the head midline structures. We show that, beside their requirement for EGFR signaling, head and ventral midline structures share several morphogenetic and molecular properties.

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Cooperation of BMP7 and SHH in the Induction of Forebrain Ventral Midline Cells by Prechordal Mesoderm

Cell ◽

10.1016/s0092-8674(00)80334-7 ◽

1997 ◽

Vol 90 (2) ◽

pp. 257-269 ◽

Cited By ~ 179

Author(s):

J.Kim Dale ◽

Christine Vesque ◽

Thierry J Lints ◽

T.Kuber Sampath ◽

Andrew Furley ◽

...

Keyword(s):

Ventral Midline ◽

Prechordal Mesoderm ◽

Midline Cells

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Lithium changes the ectodermal fate of individual frog blastomeres because it causes ectopic neural plate formation

Development ◽

10.1242/dev.106.3.599 ◽

1989 ◽

Vol 106 (3) ◽

pp. 599-610

Author(s):

S.L. Klein ◽

S.A. Moody

Keyword(s):

Neural Plate ◽

Early Cleavage ◽

Ventral Midline ◽

Plate Formation ◽

Form Part ◽

Cleavage Stages ◽

Midline Cells ◽

The Brain ◽

Brain Examination ◽

Developmental Window

Amphibian blastulae that are treated with lithium (Li) develop into embryos that consist almost exclusively of head structures. This dramatic change in embryogenesis may occur either because Li selectively kills trunk progenitors or because Li causes trunk progenitors to become head progenitors. To distinguish between these possibilities, we compared the fates of individual frog blastomeres between Li-treated embryos and normal embryos using lineage tracers. The results demonstrate that Li causes ventral midline cells, which normally populate large amounts of trunk, to produce many head structures, including the brain. Examination of fluorescently labeled clones in living Li-treated gastrulae shows that: (1) the ectodermal members of the clones migrate normally, and chordamesodermal involution begins normally; (2) the chordamesoderm's later involution is altered such that it is confined to the vegetal hemisphere; (3) accordingly, the neural plate forms in the vegetal hemisphere, circumscribing the blastopore, which normally gives rise to the cloaca; and (4) the ectodermal progeny of the ventral midline blastomeres that are near the blastopore populate the brain because they are induced by the stalled chordamesoderm to form part of the ectopic neural plate. These results demonstrate that Li, administered during a short developmental window at early cleavage stages, ultimately alters ectodermal fate because it changes the pattern of chordamesodermal involution during gastrulation, which in turn changes the site of neural plate formation.

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Development of branchiomotor neurons in zebrafish

Development ◽

10.1242/dev.124.13.2633 ◽

1997 ◽

Vol 124 (13) ◽

pp. 2633-2644 ◽

Cited By ~ 7

Author(s):

A. Chandrasekhar ◽

C.B. Moens ◽

J.T. Warren ◽

C.B. Kimmel ◽

J.Y. Kuwada

Keyword(s):

Cell Migration ◽

Neural Tube ◽

Zebrafish Embryo ◽

Mutational Analysis ◽

Ventral Midline ◽

Neuronal Specification ◽

Motor Nuclei ◽

Midline Cells ◽

Insight Into

The mechanisms underlying neuronal specification and axonogenesis in the vertebrate hindbrain are poorly understood. To address these questions, we have employed anatomical methods and mutational analysis to characterize the branchiomotor neurons in the zebrafish embryo. The zebrafish branchiomotor system is similar to those in the chick and mouse, except for the location of the nVII and nIX branchiomotor neurons. Developmental analyses of genes expressed by branchiomotor neurons suggest that the different location of the nVII neurons in the zebrafish may result from cell migration. To gain insight into the mechanisms underlying the organization and axonogenesis of these neurons, we examined the development of the branchiomotor pathways in neuronal mutants. The valentino b337 mutation blocks the formation of rhombomeres 5 and 6, and severely affects the development of the nVII and nIX motor nuclei. The cyclops b16 mutation deletes ventral midline cells in the neural tube, and leads to a severe disruption of most branchiomotor nuclei and axon pathways. These results demonstrate that rhombomere-specific cues and ventral midline cells play important roles in the development of the branchiomotor pathways.

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Sim2 Mutants Have Developmental Defects Not Overlapping with Those of Sim1 Mutants

Molecular and Cellular Biology ◽

10.1128/mcb.22.12.4147-4157.2002 ◽

2002 ◽

Vol 22 (12) ◽

pp. 4147-4157 ◽

Cited By ~ 38

Author(s):

Eleni Goshu ◽

Hui Jin ◽

Rachel Fasnacht ◽

Mike Sepenski ◽

Jacques L. Michaud ◽

...

Keyword(s):

Genetic Interaction ◽

Expression Patterns ◽

Gene Mutations ◽

Congenital Scoliosis ◽

Developmental Defects ◽

Lung Inflation ◽

Left And Right ◽

Temporal And Spatial ◽

Cns Midline ◽

Midline Cells

ABSTRACT The mouse genome contains two Sim genes, Sim1 and Sim2. They are presumed to be important for central nervous system (CNS) development because they are homologous to the Drosophila single-minded (sim) gene, mutations in which cause a complete loss of CNS midline cells. In the mammalian CNS, Sim2 and Sim1 are coexpressed in the paraventricular nucleus (PVN). While Sim1 is essential for the development of the PVN (J. L. Michaud, T. Rosenquist, N. R. May, and C.-M. Fan, Genes Dev. 12:3264-3275, 1998), we report here that Sim2 mutant has a normal PVN. Analyses of the Sim1 and Sim2 compound mutants did not reveal obvious genetic interaction between them in PVN histogenesis. However, Sim2 mutant mice die within 3 days of birth due to lung atelectasis and breathing failure. We attribute the diminished efficacy of lung inflation to the compromised structural components surrounding the pleural cavity, which include rib protrusions, abnormal intercostal muscle attachments, diaphragm hypoplasia, and pleural mesothelium tearing. Although each of these structures is minimally affected, we propose that their combined effects lead to the mechanical failure of lung inflation and death. Sim2 mutants also develop congenital scoliosis, reflected by the unequal sizes of the left and right vertebrae and ribs. The temporal and spatial expression patterns of Sim2 in these skeletal elements suggest that Sim2 regulates their growth and/or integrity.

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