scholarly journals Cytoskeletal Associated Filamin A and RhoA Affect Neural Progenitor Specification During Mitosis

2018 ◽  
Vol 29 (3) ◽  
pp. 1280-1290 ◽  
Author(s):  
Gewei Lian ◽  
Timothy Wong ◽  
Jie Lu ◽  
Jianjun Hu ◽  
Jingping Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Fate ◽  
Rho Gtpase ◽  
Brain Size ◽  
Neural Progenitor ◽  
Actin Binding ◽  
Cell Fate Specification ◽  
Filamin A ◽  
Fate Specification ◽  
M Phase

Abstract Neural progenitor proliferation and cell fate decision from self-renewal to differentiation are crucial factors in determining brain size and morphology. The cytoskeletal dependent regulation of these processes is not entirely known. The actin-binding filamin A (FlnA) was shown to regulate proliferation of progenitors by directing changes in cell cycles proteins such as Cdk1 during G2/M phase. Here we report that functional loss of FlnA not only affects the rate of proliferation by altering cell cycle length but also causes a defect in early differentiation through changes in cell fate specification. FlnA interacts with Rho GTPase RhoA, and FlnA loss impairs RhoA activation. Disruption of either of these cytoskeletal associated proteins delays neurogenesis and promotes neural progenitors to remain in proliferative states. Aurora kinase B (Aurkb) has been implicated in cytokinesis, and peaks in expression during the G2/M phase. Inhibition of FlnA or RhoA impairs Aurkb degradation and alters its localization during mitosis. Overexpression of Aurkb replicates the same delay in neurogenesis seen with loss of FlnA or RhoA. Our findings suggest that shared cytoskeletal processes can direct neural progenitor proliferation by regulating the expression and localization of proteins that are implicated in the cell cycle progression and cell fate specification.

Single cell transplantation reveals interspecific cell communication in Drosophila chimeras

Development ◽  
1990 ◽  
Vol 109 (4) ◽  
pp. 821-832 ◽  
Author(s):  
T. Becker ◽  
G.M. Technau
Keyword(s):  
Cell Cycle ◽  
Single Cell ◽  
Cell Size ◽  
Cell Fate ◽  
Cell Communication ◽  
Host Tissue ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Common Strategy ◽  
Invertebrate Development

Cell-cell communication is not only a common strategy for cell fate specification in vertebrates, but plays important roles in invertebrate development as well. We report here on experiments testing the compatibility of mechanisms specifying cell fate among six different Drosophila species. Following interspecific transplantation, the development of single ectodermal cells was traced in order to test their abilities to proliferate and differentiate in a heterologous environment. Despite considerable differences in cell size and length of cell cycle among some of the species, the transplants gave rise to fully differentiated clones that were integrated into the host tissue. Clones comprised cells of epidermal and/or neural histotypes, indicating that mechanisms mediating the epidermal/neural dichotomy in the ectoderm are conserved between the species. Cells of the neural lineages differentiated into neurones, glia, or both. Moreover, heterologous neurones sent out axons that followed major pathways along nerves and within the neuropile, demonstrating their ability to recognize positional cues in the heterologous CNS of the host.

Cell fate specification by even-skipped expression in the Drosophila nervous system is coupled to cell cycle progression

Development ◽  
1995 ◽  
Vol 121 (11) ◽  
pp. 3713-3721 ◽  
Author(s):  
K. Weigmann ◽  
C.F. Lehner
Keyword(s):  
Cell Cycle ◽  
Nervous System ◽  
Cell Fate ◽  
Mother Cell ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Cell Fate Specification ◽  
Cycle Progression ◽  
Fate Specification ◽  
Ganglion Mother Cell

The correct specification of defined neurons in the Drosophila central nervous system is dependent on even-skipped. During CNS development, even-skipped expression starts in the ganglion mother cell resulting from the first asymmetric division of neuroblast NB 1–1. This first division of NB 1–1 (and of the other early neuroblasts as well) is temporally controlled by the transcriptional regulation of string expression, which we have manipulated experimentally, even-skipped expression still occurs if the first neuroblast division is delayed, but not if the division is prohibited. Moreover, even-skipped expression is also dependent on progression through S phase which follows immediately after the first division. However, cytokinesis during the first NB division is not required for even-skipped expression as revealed by observations in pebble mutant embryos. Our results demonstrate therefore that even-skipped expression is coupled to cell cycle progression, presumably in order to prevent a premature activation of expression by a positive regulator which is produced already in the neuroblast during G2 and segregated asymmetrically into the ganglion mother cell during mitosis.

scholarly journals ARS2 is required for retinal progenitor cell S-phase progression and Müller glial cell fate specification

2020 ◽  
Vol 98 (1) ◽  
pp. 50-60 ◽  
Author(s):  
Connor O’Sullivan ◽  
Philip E.B. Nickerson ◽  
Oliver Krupke ◽  
Jennifer Christie ◽  
Li-Li Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Cell Fate Specification ◽  
Retinal Progenitor Cells ◽  
Cycle Progression ◽  
Fate Specification ◽  
Retinal Progenitor

During a developmental period that extends postnatally in the mouse, proliferating multipotent retinal progenitor cells produce one of 7 major cell types (rod, cone, bipolar, horizontal, amacrine, ganglion, and Müller glial cells) as they exit the cell cycle in consecutive waves. Cell production in the retina is tightly regulated by intrinsic, extrinsic, spatial, and temporal cues, and is coupled to the timing of cell cycle exit. Arsenic-resistance protein 2 (ARS2, also known as SRRT) is a component of the nuclear cap-binding complex involved in RNA Polymerase II transcription, and is required for cell cycle progression. We show that postnatal retinal progenitor cells (RPCs) require ARS2 for proper progression through S phase, and ARS2 disruption leads to early exit from the cell cycle. Furthermore, we observe an increase in the proportion of cells expressing a rod photoreceptor marker, and a loss of Müller glia marker expression, indicating a role for ARS2 in regulating cell fate specification or differentiation. Knockdown of Flice Associated Huge protein (FLASH), which interacts with ARS2 and is required for cell cycle progression and 3′-end processing of replication-dependent histone transcripts, phenocopies ARS2 knockdown. These data implicate ARS2–FLASH-mediated histone mRNA processing in regulating RPC cell cycle kinetics and neuroglial cell fate specification during postnatal retinal development.

scholarly journals Cell cycle independent role of Cyclin E during neural cell fate specification in Drosophila is mediated by its regulation of Prospero function

2010 ◽  
Vol 337 (2) ◽  
pp. 415-424 ◽  
Author(s):  
Christian Berger ◽  
Ramakrishnan Kannan ◽  
Sudharani Myneni ◽  
Simone Renner ◽  
L.S. Shashidhara ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Fate ◽  
Cyclin E ◽  
Neural Cell ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Neural Cell Fate

Sox proteins: regulators of cell fate specification and differentiation

Development ◽  
2013 ◽  
Vol 140 (20) ◽  
pp. 4129-4144 ◽  
Author(s):  
Y. Kamachi ◽  
H. Kondoh
Keyword(s):  
Cell Fate ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Sox Proteins
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