scholarly journals ES cell-derived presomitic mesoderm-like tissues for analysis of synchronized oscillations in the segmentation clock

Development ◽  
2018 ◽  
Vol 145 (4) ◽  
pp. dev156836 ◽  
Author(s):  
Marina Matsumiya ◽  
Takehito Tomita ◽  
Kumiko Yoshioka-Kobayashi ◽  
Akihiro Isomura ◽  
Ryoichiro Kageyama
Keyword(s):  
Es Cell ◽  
Presomitic Mesoderm ◽  
Segmentation Clock

Modeling of segmentation clock mechanism in presomitic mesoderm

2009 ◽  
Author(s):  
A. Kazama ◽  
A. Karashima ◽  
N. Katayama ◽  
M. Nakao
Keyword(s):  
Presomitic Mesoderm ◽  
Segmentation Clock ◽  
Clock Mechanism

scholarly journals PAPC couples the Segmentation Clock to somite morphogenesis by regulating N-cadherin dependent adhesion

2016 ◽  
Author(s):  
Jerome Chal ◽  
Charlene Guillot ◽  
Olivier Pourquie
Keyword(s):  
Mouse Embryos ◽  
Loss Of Function ◽  
Presomitic Mesoderm ◽  
Segmentation Clock ◽  
Anterior Compartment ◽  
Chicken Embryos ◽  
Differential Adhesion ◽  
Complementary Pattern ◽  
The Future

Vertebrate segmentation is characterized by the periodic formation of epithelial somites from the mesenchymal presomitic mesoderm (PSM). How the rhythmic signaling pulse delivered by the Segmentation Clock is translated into the periodic morphogenesis of somites remains poorly understood. Here, we focused on the role of Paraxial protocadherin (PAPC/Pcdh8) in this process. We show that in chicken and mouse embryos, PAPC expression is tightly regulated by the Clock and Wavefront system in the posterior PSM. We observed that PAPC exhibits a striking complementary pattern to N-Cadherin (CDH2), marking the interface of the future somite boundary in the anterior PSM. Gain and loss of function of PAPC in chicken embryos disrupt somite segmentation by altering the CDH2-dependent epithelialization of PSM cells. Our data suggest that clathrin-mediated endocytosis is increased in PAPC expressing cells, subsequently affecting CDH2 internalization in the anterior compartment of the future somite. This in turn generates a differential adhesion interface, allowing formation of the acellular fissure that defines the somite boundary. Thus periodic expression of PAPC downstream of the Segmentation Clock triggers rhythmic endocytosis of CDH2, allowing for segmental de-adhesion and individualization of somites.

scholarly journals Segmentation-clock synchronization in circular-lattice networks of embryonic presomitic-mesoderm cells

2021 ◽  
Vol 6 (6) ◽  
pp. 5817-5836
Author(s):  
Jesús Pantoja-Hernández ◽  
◽  
Moisés Santillán
Keyword(s):  
Clock Synchronization ◽  
Presomitic Mesoderm ◽  
Segmentation Clock

scholarly journals Axial skeletal defects caused by mutation in the spondylocostal dysplasia/pudgy geneDll3are associated with disruption of the segmentation clock within the presomitic mesoderm

Development ◽  
2002 ◽  
Vol 129 (7) ◽  
pp. 1795-1806 ◽  
Author(s):  
Sally L. Dunwoodie ◽  
Melanie Clements ◽  
Duncan B. Sparrow ◽  
Xin Sa ◽  
Ronald A. Conlon ◽  
...  
Keyword(s):  
Gene Targeting ◽  
Skeletal Dysplasia ◽  
Null Allele ◽  
Developmental Origins ◽  
Loss Of Function ◽  
Presomitic Mesoderm ◽  
Phenotypic Analysis ◽  
Segmentation Clock ◽  
Skeletal Defects ◽  
Somite Formation

A loss-of-function mutation in the mouse delta-like3 (Dll3) gene has been generated following gene targeting, and results in severe axial skeletal defects. These defects, which consist of highly disorganised vertebrae and costal defects, are similar to those associated with the Dll3-dependent pudgy mutant in mouse and with spondylocostal dysplasia (MIM 277300) in humans. This study demonstrates that Dll3neo and Dll3pu are functionally equivalent alleles with respect to the skeletal dysplasia, and we suggest that the three human DLL3 mutations associated with spondylocostal dysplasia are also functionally equivalent to the Dll3neo null allele. Our phenotypic analysis of Dll3neo/Dll3neo mutants shows that the developmental origins of the skeletal defects lie in delayed and irregular somite formation, which results in the perturbation of anteroposterior somite polarity. As the expression of Lfng, Hes1, Hes5 and Hey1 is disrupted in the presomitic mesoderm, we suggest that the somitic aberrations are founded in the disruption of the segmentation clock that intrinsically oscillates within presomitic mesoderm.

scholarly journals Real-time imaging of the somite segmentation clock: Revelation of unstable oscillators in the individual presomitic mesoderm cells

2006 ◽  
Vol 103 (5) ◽  
pp. 1313-1318 ◽  
Author(s):  
Y. Masamizu ◽  
T. Ohtsuka ◽  
Y. Takashima ◽  
H. Nagahara ◽  
Y. Takenaka ◽  
...  
Keyword(s):  
Real Time ◽  
Presomitic Mesoderm ◽  
Segmentation Clock ◽  
Real Time Imaging ◽  
The Individual

scholarly journals Intrinsic noise, Delta-Notch signalling and delayed reactions promote sustained, coherent, synchronized oscillations in the presomitic mesoderm

2019 ◽  
Vol 16 (160) ◽  
pp. 20190436 ◽  
Author(s):  
Joseph W. Baron ◽  
Tobias Galla
Keyword(s):  
Gene Expression ◽  
Intrinsic Noise ◽  
Active Role ◽  
Notch Signalling ◽  
Presomitic Mesoderm ◽  
Segmentation Clock ◽  
Sustained Oscillations ◽  
Stochastic Waves ◽  
Delayed Reactions ◽  
Modelling Approach

Using a stochastic individual-based modelling approach, we examine the role that Delta-Notch signalling plays in the regulation of a robust and reliable somite segmentation clock. We find that not only can Delta-Notch signalling synchronize noisy cycles of gene expression in adjacent cells in the presomitic mesoderm (as is known), but it can also amplify and increase the coherence of these cycles. We examine some of the shortcomings of deterministic approaches to modelling these cycles and demonstrate how intrinsic noise can play an active role in promoting sustained oscillations, giving rise to noise-induced quasi-cycles. Finally, we explore how translational/transcriptional delays can result in the cycles in neighbouring cells oscillating in anti-phase and we study how this effect relates to the propagation of noise-induced stochastic waves.

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