scholarly journals A Nodal/Eph signalling relay drives the transition from apical constriction to apico-basal shortening in ascidian endoderm invagination

Development ◽  
2020 ◽  
Vol 147 (15) ◽  
pp. dev186965
Author(s):  
Ulla-Maj Fiuza ◽  
Takefumi Negishi ◽  
Alice Rouan ◽  
Hitoyoshi Yasuo ◽  
Patrick Lemaire
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Ciona Intestinalis ◽  
Precursor Cells ◽  
Endodermal Cell ◽  
Apical Constriction ◽  
Fate Specification ◽  
Endoderm Cell ◽  
Ascidian Species ◽  
Morphogenetic Event

ABSTRACTGastrulation is the first major morphogenetic event during animal embryogenesis. Ascidian gastrulation starts with the invagination of 10 endodermal precursor cells between the 64- and late 112-cell stages. This process occurs in the absence of endodermal cell division and in two steps, driven by myosin-dependent contractions of the acto-myosin network. First, endoderm precursors constrict their apex. Second, they shorten apico-basally, while retaining small apical surfaces, thereby causing invagination. The mechanisms that prevent endoderm cell division, trigger the transition between step 1 and step 2, and drive apico-basal shortening have remained elusive. Here, we demonstrate a conserved role for Nodal and Eph signalling during invagination in two distantly related ascidian species, Phallusia mammillata and Ciona intestinalis. Specifically, we show that the transition to step 2 is triggered by Nodal relayed by Eph signalling. In addition, our results indicate that Eph signalling lengthens the endodermal cell cycle, independently of Nodal. Finally, we find that both Nodal and Eph signals are dispensable for endoderm fate specification. These results illustrate commonalities as well as differences in the action of Nodal during ascidian and vertebrate gastrulation.

scholarly journals A Nodal/Eph signalling relay drives the transition from apical constriction to apico-basal shortening in ascidian endoderm invagination

2018 ◽  
Author(s):  
Ulla-Maj Fiuza ◽  
Takefumi Negishi ◽  
Alice Rouan ◽  
Hitoyoshi Yasuo ◽  
Patrick Lemaire
Keyword(s):  
Cell Fate ◽  
Cell Fate Specification ◽  
Apical Constriction ◽  
Fate Specification ◽  
Mitotic Delay ◽  
Ascidian Species ◽  
Morphogenetic Event ◽  
Summary Statement ◽  
Developmental Signalling ◽  
Shape Changes

AbstractGastrulation is the first major morphogenetic event during animal embryogenesis. Ascidian gastrulation starts with the invagination of 10 endodermal precursor cells between the 64- and late 112-cell stages. This process occurs in the absence of endodermal cell division and in two steps, driven by myosin-dependent contractions of the acto-myosin network. First, endoderm precursors constrict their apex. Second, they shorten apico-basally, while retaining small apical surfaces, thereby causing invagination. The mechanisms controlling the endoderm mitotic delay, the step 1 to step 2 transition, and apico-basal shortening have remained elusive. Here, we demonstrate the conserved role during invagination of Nodal and Eph signalling in two distantly related ascidian species (Phallusia mammillata and Ciona intestinalis). We show that the transition to step 2 is controlled by Nodal relayed by Eph signalling and that Eph signalling has a Nodal-independent role in mitotic delay. Interestingly, both Nodal and Eph signals are dispensable for endodermal germ layer fate specification.Summary statementIdentification of a regulatory developmental signalling sub-network driving endoderm cell shape changes during ascidian endoderm invagination, not involved in cell fate specification.

scholarly journals Regulation of Cell Division in Bacteria by Monitoring Genome Integrity and DNA Replication Status

2019 ◽  
Vol 202 (2) ◽  
Author(s):  
Peter E. Burby ◽  
Lyle A. Simmons
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Division ◽  
Dna Replication ◽  
Cell Cycle Progression ◽  
Genome Instability ◽  
Sos Response ◽  
Bacterial Cells ◽  
Cycle Progression ◽  
Content Type

ABSTRACT All organisms regulate cell cycle progression by coordinating cell division with DNA replication status. In eukaryotes, DNA damage or problems with replication fork progression induce the DNA damage response (DDR), causing cyclin-dependent kinases to remain active, preventing further cell cycle progression until replication and repair are complete. In bacteria, cell division is coordinated with chromosome segregation, preventing cell division ring formation over the nucleoid in a process termed nucleoid occlusion. In addition to nucleoid occlusion, bacteria induce the SOS response after replication forks encounter DNA damage or impediments that slow or block their progression. During SOS induction, Escherichia coli expresses a cytoplasmic protein, SulA, that inhibits cell division by directly binding FtsZ. After the SOS response is turned off, SulA is degraded by Lon protease, allowing for cell division to resume. Recently, it has become clear that SulA is restricted to bacteria closely related to E. coli and that most bacteria enforce the DNA damage checkpoint by expressing a small integral membrane protein. Resumption of cell division is then mediated by membrane-bound proteases that cleave the cell division inhibitor. Further, many bacterial cells have mechanisms to inhibit cell division that are regulated independently from the canonical LexA-mediated SOS response. In this review, we discuss several pathways used by bacteria to prevent cell division from occurring when genome instability is detected or before the chromosome has been fully replicated and segregated.

scholarly journals Anticancer potential of nitric oxide (NO) in neuroblastoma treatment

RSC Advances ◽  
2021 ◽  
Vol 11 (16) ◽  
pp. 9112-9120
Author(s):  
Jenna L. Gordon ◽  
Kristin J. Hinsen ◽  
Melissa M. Reynolds ◽  
Tyler A. Smith ◽  
Haley O. Tucker ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Cycle ◽  
Cell Division ◽  
Cell Viability ◽  
Cell Cycle Arrest ◽  
Neuroblastoma Cells ◽  
Cycle Arrest

S-Nitrosoglutathione (GSNO) reduces cell viability, inhibits cell division, and induces cell cycle arrest and apoptosis in neuroblastoma cells.

scholarly journals The Pericardial Body of Ciona intestinalis Contains Hemocytes and Degenerating Muscle Cells, But No Parasites

2020 ◽  
Author(s):  
Lilly Rohlfs ◽  
Katja Müller ◽  
Thomas Stach
Keyword(s):  
Immune System ◽  
Model Organism ◽  
Gene Sequencing ◽  
Ciona Intestinalis ◽  
Sister Group ◽  
Myocardial Cells ◽  
Histological Techniques ◽  
Transmission Electron ◽  
Ascidian Species ◽  
Competing Hypotheses

Abstract Purpose A ventral heart positioned posterior to the branchial basket and equipped with a pericardium is homologous in tunicates and their sister group, the craniates, yet the tunicate model organism Ciona intestinalis features a pericardial body, a structure peculiar to few ascidian species. Here, we set out to distinguish between two competing hypotheses regarding the function of the pericardial body found in the literature: (H1) The pericardial body performs a role in the removal of dysfunctional myocardial cells, and (H2) it is a specialized niche of the immune system involved in defense against parasites. Methods We used histological techniques, transmission electron microscopy, and PCR-based gene sequencing to investigate whether individual ascidians parasitized with apicomplexan protists show signs of infections within the pericardial body. Results In individuals of C. intestinalis from the German North Sea infested with apicomplexan protists, the pericardial body contains numerous myocardial cells in various stages of degeneration while no remnants of parasitic cells could be identified. Conclusion Thus, we conclude that H2—the pericardial body is a specialized niche of the immune system involved in defense against parasites—can be refuted. Rather, our observations support H1, the hypothesis that the pericardial body performs a role in the removal of dysfunctional myocardial cells.

Sign in / Sign up

Export Citation Format

Share Document