scholarly journals Myc activity is required for maintenance of the neuromesodermal progenitor signalling network and for segmentation clock gene oscillations in mouse

Development ◽  
2018 ◽  
Vol 145 (14) ◽  
pp. dev161091 ◽  
Author(s):  
Ioanna Mastromina ◽  
Laure Verrier ◽  
Joana Clara Silva ◽  
Kate G. Storey ◽  
J. Kim Dale
Keyword(s):  
Clock Gene ◽  
Segmentation Clock ◽  
Signalling Network ◽  
Segmentation Clock Gene

scholarly journals Greb1 is required for axial elongation and segmentation in vertebrate embryos

2019 ◽  
Author(s):  
Ravindra Singh Prajapati ◽  
Richard Mitter ◽  
Annalisa Vezzaro ◽  
David Ish-Horowicz
Keyword(s):  
Estrogen Receptor ◽  
Embryonic Development ◽  
Clock Gene ◽  
Zebrafish Embryos ◽  
Presomitic Mesoderm ◽  
Axial Elongation ◽  
No Tail ◽  
Vertebrate Embryos ◽  
Progenitor Maintenance ◽  
Segmentation Clock Gene

ABSTRACTDuring vertebrate embryonic development, the formation of axial structures is driven by a population of stem-like cells that reside in a region of the tailbud called the chordoneural hinge (CNH). We have compared the CNH transcriptome with those of surrounding tissues and shown that the CNH and tailbud mesoderm are transcriptionally similar, and distinct from the presomitic mesoderm. Amongst CNH-enriched genes are several that are required for axial elongation, including Wnt3a, Cdx2, Brachyury/T and Fgf8, and androgen/estrogen receptor nuclear signalling components such as Greb1. We show that the pattern and duration of tailbud Greb1 expression is conserved in mouse, zebrafish, and chicken embryos, and that Greb1 is required for axial elongation and somitogenesis in zebrafish embryos. The axial truncation phenotype of Greb1 morphant embryos is explained by much reduced expression of No tail (Ntl/Brachyury) which is required for axial progenitor maintenance. Posterior segmentation defects in the morphants (including misexpression of genes such as mespb, myoD and papC) appear to result, in part, from lost expression of the segmentation clock gene, her7.

scholarly journals Fibronectin-dependent tissue mechanics regulate the translation of segmentation clock oscillations into periodic somite formation

2019 ◽  
Author(s):  
Patrícia Gomes de Almeida ◽  
Pedro Rifes ◽  
Ana Patrícia Martins-Jesus ◽  
Gonçalo G. Pinheiro ◽  
Raquel P. Andrade ◽  
...  
Keyword(s):  
Gene Expression ◽  
Clock Gene ◽  
Clock Genes ◽  
Tissue Mechanics ◽  
Matrix Assembly ◽  
Segmentation Clock ◽  
Clock Gene Expression ◽  
Fibronectin Matrix ◽  
Somite Formation ◽  
Spatio Temporal

AbstractSomitogenesis starts with cyclic waves of expression of segmentation clock genes in the presomitic mesoderm (PSM) and culminates with periodic budding of somites in its anterior-most region. How cyclic clock gene expression is translated into timely morphological somite formation has remained unclear. A posterior to anterior gradient of increasing PSM tissue cohesion correlates with increasing fibronectin matrix complexity around the PSM, suggesting that fibronectin-dependent tissue mechanics may be involved in this transition. Here we address whether the mechanical properties of the PSM tissue play a role in regulating the pathway leading to cleft formation in the anterior PSM. We first interfered with cytoskeletal contractility in the chick PSM by disrupting actomyosin-mediated contractility directly or via Rho-associated protein kinase function. Then we perturbed fibronectin matrix accumulation around the PSM tissue by blocking integrin-fibronectin binding or fibronectin matrix assembly. All four treatments perturbed hairy1 and meso1 expression dynamics and resulted in defective somitic clefts. A model is presented where a gradient of fibronectin-dependent tissue mechanics participates in the PSM wavefront of maturation by ensuring the correct spatio-temporal conversion of cyclic segmentation clock gene expression into periodic somite formation.

scholarly journals CLOCK/BMAL1 interferes with segmentation clock oscillation in mouse embryonic organoids

2020 ◽  
Author(s):  
Yasuhiro Umemura ◽  
Nobuya Koike ◽  
Yoshiki Tsuchiya ◽  
Hitomi Watanabe ◽  
Gen Kondoh ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Clock Gene ◽  
Developmental Process ◽  
Biological Significance ◽  
Sequencing Analysis ◽  
Mammalian Development ◽  
Segmentation Clock ◽  
Interest Statement ◽  
Competing Interest ◽  
Clear Information

AbstractIn the mammalian developmental process, the segmentation clock and circadian clock appear sequentially in the embryo. However, there is no clear information about the biological significance of the mutual exclusiveness of these rhythms. Here we show that excess of the circadian components CLOCK/BMAL1 in mouse embryonic organoids, induced presomitic mesoderm and gastruloids, disrupts the Hes7 ultradian rhythm and somitogenesis. RNA sequencing analysis showed that CLOCK/BMAL1 activates the signaling pathways regulating Hes7. After establishment of the circadian clock, the expression of endogenous Hes7 and another segmentation clock gene, Lfng, tended to fluctuate with a circadian period, implying that the circadian clock potentially interferes with the segmentation clock. These results suggest that strict timing regulation of the emergence of circadian clock oscillation is essential for mammalian development.Competing Interest StatementThe authors have declared no competing interest.

scholarly journals CDK1 and CDK2 regulate phosphorylation-dependent NICD1 turnover and the periodicity of the segmentation clock

2018 ◽  
Author(s):  
Francesca Anna Carrieri ◽  
Philip Murray ◽  
Paul Davies ◽  
Jacqueline Kim Dale
Keyword(s):  
Clock Gene ◽  
Dependent Manner ◽  
Clock Period ◽  
Segmentation Clock ◽  
Clock Gene Expression ◽  
Notch Intracellular Domain ◽  
Somite Formation ◽  
Cycle Dependent

ABSTRACTAll vertebrates share a segmented body axis. Segments form periodically from the rostral end of the presomitic mesoderm (PSM) and this periodicity is regulated by the segmentation clock, a molecular oscillator that drives dynamic clock gene expression across the PSM with a periodicity that matches somite formation. Notch signalling is crucial to this process. Altering Notch intracellular domain (NICD) stability affects both the clock period and somite size. However, the mechanistic details of how NICD stability is regulated are unclear.We identified a highly conserved site crucial for NICD recognition by the SCF E3 ligase, which targets NICD for degradation. We demonstrate both CDK1 and CDK2 can phosphorylate NICD in the domain where this crucial residue lies and that NICD levels vary in a cell cycle-dependent manner. Inhibiting CDK1 or CDK2 activity increases NICD levels both in vitro and in vivo, leading to a delay of clock gene oscillations.

scholarly journals MYC activity is required for maintenance of the Neuromesodermal Progenitor signalling network and for correct timing of segmentation clock gene oscillations

2017 ◽  
Author(s):  
Ioanna Mastromina ◽  
Laure Verrier ◽  
Kate G. Storey ◽  
J. Kim Dale
Keyword(s):  
Cell Cycle Progression ◽  
The Body ◽  
Body Axis ◽  
Cellular Functions ◽  
Segmentation Clock ◽  
Signalling Network ◽  
Undifferentiated State ◽  
Somite Formation ◽  
Axis Elongation ◽  
And Function

AbstractThe Myc transcriptional regulators are implicated in a range of cellular functions, including proliferation, cell cycle progression, metabolism and pluripotency maintenance. Here, we investigated the expression, regulation and function of Myc during mouse embryonic axis elongation and segmentation. Expression of both cMyc and MycN in the domains where neuromesodermal progenitors (NMPs) and underlying caudal pre-somitic mesoderm (cPSM) cells reside is coincident WNT and FGF signals; factors known to maintain progenitors in an undifferentiated state. Pharmacological inhibition of MYC activity, downregulates expression of WNT/FGF components. In turn, we find that cMyc expression is WNT, FGF and NOTCH regulated, placing it centrally in the signalling circuit that operates in the tail end that both sustains progenitors and drives maturation of the PSM into somites. Interfering with MYC function in the PSM, where it displays oscillatory expression, delays the timing of segmentation clock oscillations and thus of somite formation. In summary, we identify Myc as a component that links NMP maintenance and PSM maturation during the body axis elongation stages of mouse embryogenesis.Summary StatementMYC operates in a positive feedback loop with WNT/FGF signals to maintain the progenitors which facilitate body axis elongation while its activity is crucial for timing of the segmentation clock.

The chicken CLOCK gene maps to chromosome 4

2000 ◽  
Vol 31 (5) ◽  
pp. 344-344 ◽  
Author(s):  
M A Noakes ◽  
M T Campbell ◽  
B J Van Hest
Keyword(s):  
Clock Gene ◽  
Chromosome 4 ◽  
Gene Maps
Sign in / Sign up

Export Citation Format

Share Document