A role for CK2 upon interkinetic nuclear migration in the cell cycle of retinal progenitor cells

2008 ◽  
Vol 68 (5) ◽  
pp. 620-631 ◽  
Author(s):  
Ana Carolina Dudenhoeffer Carneiro ◽  
Lucianne Fragel-Madeira ◽  
Mario Alberto Silva-Neto ◽  
Rafael Linden
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Nuclear Migration ◽  
Retinal Progenitor Cells ◽  
Retinal Progenitor ◽  
Interkinetic Nuclear Migration

scholarly journals Cephalopod Retinal Development Shows Vertebrate-like Mechanisms of Neurogenesis

2021 ◽  
Author(s):  
Francesca Napoli ◽  
Christina M Daly ◽  
Stephanie Neal ◽  
Kyle J McCulloch ◽  
Alexandra Zaloga ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nervous System ◽  
Progenitor Cells ◽  
Cellular Proliferation ◽  
Imaging Techniques ◽  
Nuclear Migration ◽  
Live Imaging ◽  
Cellular Mechanisms ◽  
High Resolution Data ◽  
Interkinetic Nuclear Migration

Neurogenesis, the regulation of cellular proliferation and differentiation in the developing nervous system, is the process that underlies the diversity of size and cell type found in animal nervous systems. Our understanding of how this process has evolved is limited because of the lack of high resolution data and live-imaging methods across species. The retina is a classic model for the study of neurogenesis in vertebrates and live-imaging of the retina has shown that during development, progenitor cells are organized in a pseudostratified neuroepithelium and nuclei migrate in coordination with the cell cycle along the apicobasal axis of the cell, a process called interkinetic nuclear migration. Eventually cells delaminate and differentiate within the boundaries of the epithelium. This process has been considered unique to vertebrates and thought to be important in maintaining organization during the development of a complex nervous system. Coleoid cephalopods, including squid, cuttlefish and octopus, have the largest nervous system of any invertebrate and convergently-evolved camera-type eyes, making them a compelling comparative system to vertebrates. Here we have pioneered live-imaging techniques to show that the squid, Doryteuthis pealeii, displays cellular mechanisms during cephalopod retinal neurogenesis that are hallmarks of vertebrate processes. We find that retinal progenitor cells in the squid undergo interkinetic nuclear migration until they exit the cell cycle, we identify retinal organization corresponding to progenitor, post-mitotic and differentiated cells, and we find that Notch signaling regulates this process. With cephalopods and vertebrates having diverged 550 million years ago, these results suggest that mechanisms thought to be unique to vertebrates may be common to highly proliferative neurogenic primordia contributing to a large nervous system.

p57(Kip2) regulates progenitor cell proliferation and amacrine interneuron development in the mouse retina

Development ◽  
2000 ◽  
Vol 127 (16) ◽  
pp. 3593-3605 ◽  
Author(s):  
M.A. Dyer ◽  
C.L. Cepko
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Kinase Inhibitor ◽  
Retinal Development ◽  
Cell Types ◽  
Cell Cycle Exit ◽  
Retinal Progenitor Cells ◽  
Mouse Development ◽  
Retinal Progenitor ◽  
Cyclin Kinase Inhibitor

A precise balance between proliferation and differentiation must be maintained during retinal development to obtain the correct proportion of each of the seven cell types found in the adult tissue. Cyclin kinase inhibitors can regulate cell cycle exit coincident with induction of differentiation programs during development. We have found that the p57(Kip2) cyclin kinase inhibitor is upregulated during G(1)/G(0) in a subset of retinal progenitor cells exiting the cell cycle between embryonic day 14.5 and 16.5 of mouse development. Retroviral mediated overexpression of p57(Kip2) in embryonic retinal progenitor cells led to premature cell cycle exit. Retinae from mice lacking p57(Kip2) exhibited inappropriate S-phase entry and apoptotic nuclei were found in the region where p57(Kip2) is normally expressed. Apoptosis precisely compensated for the inappropriate proliferation in the p57(Kip2)-deficient retinae to preserve the correct proportion of the major retinal cell types. Postnatally, p57(Kip2) was found to be expressed in a novel subpopulation of amacrine interneurons. At this stage, p57(Kip2)did not regulate proliferation. However, perhaps reflecting its role during this late stage of development, animals lacking p57(Kip2) showed an alteration in amacrine subpopulations. p57(Kip2) is the first gene to be implicated as a regulator of amacrine subtype/subpopulation development. Consequently, we propose that p57(Kip2) has two roles during retinal development, acting first as a cyclin kinase inhibitor in mitotic progenitor cells, and then playing a distinct role in neuronal differentiation.

scholarly journals Pax6 Is Required for Normal Cell-Cycle Exit and the Differentiation Kinetics of Retinal Progenitor Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e76489 ◽  
Author(s):  
Chen Farhy ◽  
Michael Elgart ◽  
Zehavit Shapira ◽  
Varda Oron-Karni ◽  
Orly Yaron ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Normal Cell ◽  
Cell Cycle Exit ◽  
Retinal Progenitor Cells ◽  
Retinal Progenitor ◽  
Kinetics Of ◽  
Normal Cell Cycle

scholarly journals Notch signaling represses cone photoreceptor formation through the regulation of retinal progenitor cell states

2020 ◽  
Author(s):  
Xueqing Chen ◽  
Mark M. Emerson
Keyword(s):  
Cell Cycle ◽  
Notch Signaling ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
State Transitions ◽  
Proliferative Potential ◽  
Primary Role ◽  
Cone Photoreceptor ◽  
Retinal Progenitor Cells ◽  
Retinal Progenitor

AbstractVertebrate cone photoreceptor formation is a multistep process. First, multipotent retinal progenitor cells generate genetically-defined restricted/neurogenic progenitor cells and these cells then divide to preferentially produce cones and horizontal cells. Notch signaling represses cone formation and maintains the proliferative potential of retinal progenitor cells. However, the mechanisms through which it affects these processes are unknown. Here we use cell type specific inhibition of Notch signaling to localize the primary role of Notch signaling during cone genesis to the regulation of restricted retinal progenitor cells from multipotent retinal progenitor cells. Notch signaling inhibition in restricted progenitor cells does not alter the number of cones derived from these cells but does affect horizontal cell development. Cell cycle promotion is not a primary effect of Notch signaling but an indirect effect on progenitor cell state transitions that leads to depletion of the multipotent progenitor cell population. Taken together, this suggests that the roles of Notch in cone photoreceptor formation and cell cycle promotion are both mediated by a localized function in multipotent retinal progenitor cells to repress the formation of restricted progenitor cells.

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 Loss of Nance-Horan Syndrome b (nhsb) prevents expansion growth of retinal progenitor cells by selective up-regulation of Δ113p53

2019 ◽  
Author(s):  
Paul J. Vorster ◽  
John Ojumu ◽  
Amanda J. G. Dickinson ◽  
Gregory S. Walsh
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Negative Regulator ◽  
Loss Of Function ◽  
Retinal Progenitor Cells ◽  
Cycle Progression ◽  
Retinal Progenitor ◽  
Eye Size ◽  
Regulation Of Cell Cycle

AbstractThe regulation of cell cycle progression and differentiation in retinal progenitor cells is a fundamental feature controlling organ size of the eye in vertebrates. Nance-Horan Syndrome (NHS) is a rare X-linked disorder caused by mutations in the NHS gene. Dysmorphic features of NHS include severe congenital cataracts, micropthalmia, facial dysmorphisms, and visual impairment. In this study we report an evolutionarily conserved role for NHS in vertebrate retinogenesis. Loss of function of nhs leads to small eye size in both zebrafish and Xenopus tropicalis, marked by reduced proliferation but not cell death. Transcriptome analysis of nhs morphant zebrafish eyes revealed a marked upregulation in Δ113p53, an isoform of p53, concomitant with a selective upregulation of p53 responsive genes that inhibit cell cycle progression but not apoptosis. Our data supports a model where Nhs is a negative regulator of Δ113p53 expression and exerts its function through regulation of the p53 pathway to promote expansive growth of retinal progenitor cells prior to differentiation.

Different characteristics of rat retinal progenitor cells from different culture periods

2003 ◽  
Vol 341 (3) ◽  
pp. 213-216 ◽  
Author(s):  
Tadamichi Akagi ◽  
Masatoshi Haruta ◽  
Joe Akita ◽  
Akihiro Nishida ◽  
Yoshihito Honda ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Retinal Progenitor Cells ◽  
Retinal Progenitor ◽  
Different Characteristics
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