scholarly journals Dual role for Drosophila lethal of scute in CNS midline precursor formation and dopaminergic neuron and motoneuron cell fate

Development ◽  
2011 ◽  
Vol 138 (11) ◽  
pp. 2171-2183 ◽  
Author(s):  
S. B. Stagg ◽  
A. R. Guardiola ◽  
S. T. Crews
Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 893-901 ◽  
Author(s):  
S.H. Kim ◽  
S.T. Crews

The ventral epidermis of Drosophila melanogaster is derived from longitudinal rows of ectodermal precursor cells that divide and expand to form the ventral embryonic surface. The spitz class genes are required for the proper formation of the larval ventral cuticle. Using a group of enhancer trap lines that stain subsets of epidermal cells, it is shown here that spitz class gene function is necessary for ventral epidermal development and gene expression. Analysis of single-minded mutant embryos implies that ventral epidermal cell fate is influenced by the CNS midline cells.


Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3291-3299 ◽  
Author(s):  
G. Udolph ◽  
J. Urban ◽  
G. Rusing ◽  
K. Luer ◽  
G.M. Technau

The Drosophila ventral nerve cord derives from a stereotype population of about 30 neural stem cells, the neuroblasts, per hemineuromere. Previous experiments provided indications for inductive signals at ventral sites of the neuroectoderm that confer neuroblast identities. Using cell lineage analysis, molecular markers and cell transplantation, we show here that EGF receptor signalling plays an instructive role in CNS patterning and exerts differential effects on dorsoventral subpopulations of neuroblasts. The Drosophila EGF receptor (DER) is capable of cell autonomously specifiying medial and intermediate neuroblast cell fates. DER signalling appears to be most critical for proper development of intermediate neuroblasts and less important for medial neuroblasts. It is not required for lateral neuroblast lineages or for cells to adopt CNS midline cell fate. Thus, dorsoventral patterning of the CNS involves both DER-dependent and -independent regulatory pathways. Furthermore, we discuss the possibility that different phases of DER activation exist during neuroectodermal patterning with an early phase independent of midline-derived signals.


Development ◽  
1994 ◽  
Vol 120 (8) ◽  
pp. 2143-2152 ◽  
Author(s):  
M.G. Gorczyca ◽  
R.W. Phillis ◽  
V. Budnik

During the development of peripheral nerves, pioneer axons often navigate over mesodermal tissues. In this paper, we examine the role of the mesodermal cell determination gene tinman on cells that provide pathfinding cues in Drosophila. We focus on a subset of peripheral nerves, the transverse nerves, that innervate abdominal segments. During wildtype embryonic development, the transverse nerve efferents associate with glial cells located on the dorsal aspect of the CNS midline (transverse nerve exit glia). These glial cells have cytoplasmic extensions that prefigure the transverse nerve pathway from the CNS to the body wall musculature prior to transverse nerve formation. Transverse nerve efferents extend along this scaffold to the periphery, where they fasciculate with projections from a peripheral neuron--the LBD. In tinman mutants, the transverse nerve exit glia appear to be missing, and efferent fibers remain stalled at the CNS midline, without forming transverse nerves. In addition, fibers of the LBD neurons are often truncated. These results suggest that the lack of exit glia prevents normal transverse nerve pathfinding. Another prominent defect in tinman is the loss of all dorsal neurohemal organs, FMRFamide-expressing thoracic structures which likely contain the homologs of the transverse nerve exit glia in the thoracic segments. Our results support the hypothesis that the exit glia have a mesodermal origin and that glia play an essential role in determining transverse nerve axon pathways.


Oncotarget ◽  
2015 ◽  
Vol 6 (20) ◽  
pp. 17873-17890 ◽  
Author(s):  
Paola Indovina ◽  
Francesca Pentimalli ◽  
Nadia Casini ◽  
Immacolata Vocca ◽  
Antonio Giordano

2014 ◽  
Vol 26 (7) ◽  
pp. 1385-1391 ◽  
Author(s):  
Wafa B'chir ◽  
Cédric Chaveroux ◽  
Valérie Carraro ◽  
Julien Averous ◽  
Anne-Catherine Maurin ◽  
...  

Angiogenesis ◽  
2015 ◽  
Vol 19 (1) ◽  
pp. 95-106 ◽  
Author(s):  
Chen-Wei Yu ◽  
Xiaoliang Liang ◽  
Samantha Lipsky ◽  
Cagatay Karaaslan ◽  
Harry Kozakewich ◽  
...  

2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.


2020 ◽  
Vol 64 (2) ◽  
pp. 223-232 ◽  
Author(s):  
Ben L. Carty ◽  
Elaine M. Dunleavy

Abstract Asymmetric cell division (ACD) produces daughter cells with separate distinct cell fates and is critical for the development and regulation of multicellular organisms. Epigenetic mechanisms are key players in cell fate determination. Centromeres, epigenetically specified loci defined by the presence of the histone H3-variant, centromere protein A (CENP-A), are essential for chromosome segregation at cell division. ACDs in stem cells and in oocyte meiosis have been proposed to be reliant on centromere integrity for the regulation of the non-random segregation of chromosomes. It has recently been shown that CENP-A is asymmetrically distributed between the centromeres of sister chromatids in male and female Drosophila germline stem cells (GSCs), with more CENP-A on sister chromatids to be segregated to the GSC. This imbalance in centromere strength correlates with the temporal and asymmetric assembly of the mitotic spindle and potentially orientates the cell to allow for biased sister chromatid retention in stem cells. In this essay, we discuss the recent evidence for asymmetric sister centromeres in stem cells. Thereafter, we discuss mechanistic avenues to establish this sister centromere asymmetry and how it ultimately might influence cell fate.


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