scholarly journals Hes5.9 Coordinate FGF and Notch Signaling to Modulate Gastrulation via Regulating Cell Fate Specification and Cell Migration in Xenopus tropicalis

Genes ◽  
2020 ◽  
Vol 11 (11) ◽  
pp. 1363
Author(s):  
Xiao Huang ◽  
Liyue Zhang ◽  
Shanshan Yang ◽  
Yongpu Zhang ◽  
Mingjiang Wu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Notch Signaling ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Expression Patterns ◽  
Marker Genes ◽  
Cell Fate Specification ◽  
Mesodermal Cell ◽  
Cell Fate Decisions ◽  
Fate Specification

Gastrulation drives the establishment of three germ layers and embryonic axes during frog embryonic development. Mesodermal cell fate specification and morphogenetic movements are vital factors coordinating gastrulation, which are regulated by numerous signaling pathways, such as the Wnt (Wingless/Integrated), Notch, and FGF (Fibroblast growth factor) pathways. However, the coordination of the Notch and FGF signaling pathways during gastrulation remains unclear. We identified a novel helix–loop–helix DNA binding domain gene (Hes5.9), which was regulated by the FGF and Notch signaling pathways during gastrulation. Furthermore, gain- and loss-of-function of Hes5.9 led to defective cell migration and disturbed the expression patterns of mesodermal and endodermal marker genes, thus interfering with gastrulation. Collectively, these results suggest that Hes5.9 plays a crucial role in cell fate decisions and cell migration during gastrulation, which is modulated by the FGF and Notch signaling pathways.

scholarly journals Estrogen Signaling Drives Ciliogenesis in Human Endometrial Organoids

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2282-2297 ◽  
Author(s):  
Sandra Haider ◽  
Magdalena Gamperl ◽  
Thomas R Burkard ◽  
Victoria Kunihs ◽  
Ulrich Kaindl ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Expression Patterns ◽  
Estrogen Signaling ◽  
Ciliated Cells ◽  
Cell Fate Decisions ◽  
Primary Driver ◽  
Endometrial Epithelium ◽  
Cyclic Changes

Abstract The human endometrium is the inner lining of the uterus consisting of stromal and epithelial (secretory and ciliated) cells. It undergoes a hormonally regulated monthly cycle of growth, differentiation, and desquamation. However, how these cyclic changes control the balance between secretory and ciliated cells remains unclear. Here, we established endometrial organoids to investigate the estrogen (E2)-driven control of cell fate decisions in human endometrial epithelium. We demonstrate that they preserve the structure, expression patterns, secretory properties, and E2 responsiveness of their tissue of origin. Next, we show that the induction of ciliated cells is orchestrated by the coordinated action of E2 and NOTCH signaling. Although E2 is the primary driver, inhibition of NOTCH signaling provides a permissive environment. However, inhibition of NOTCH alone is not sufficient to trigger ciliogenesis. Overall, we provide insights into endometrial biology and propose endometrial organoids as a robust and powerful model for studying ciliogenesis in vitro.

scholarly journals Scabrous overexpression in the eye affects R3/R4 cell fate specification and inhibits notch signaling

2015 ◽  
Vol 245 (2) ◽  
pp. 166-174 ◽  
Author(s):  
Verónica Muñoz-Soriano ◽  
Diego Santos ◽  
Fabrice C. Durupt ◽  
Sandra Casani ◽  
Nuria Paricio
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Cell Fate Specification ◽  
Fate Specification

scholarly journals RBP-Jκ-Dependent Notch Signaling Is Dispensable for Mouse Early Embryonic Development

2006 ◽  
Vol 26 (13) ◽  
pp. 4769-4774 ◽  
Author(s):  
Céline Souilhol ◽  
Sarah Cormier ◽  
Kenji Tanigaki ◽  
Charles Babinet ◽  
Michel Cohen-Tannoudji
Keyword(s):  
Embryonic Development ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Cell Fate ◽  
Notch Pathway ◽  
Notch Signaling Pathway ◽  
Preimplantation Embryos ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Evolutionarily Conserved

ABSTRACT The Notch signaling pathway is an evolutionarily conserved signaling system which has been shown to be essential in cell fate specification and in numerous aspects of embryonic development in all metazoans thus far studied. We recently demonstrated that several components of the Notch signaling pathway, including the four Notch receptors and their five ligands known in mammals, are expressed in mouse oocytes, in mouse preimplantation embryos, or both. This suggested a possible implication of the Notch pathway in the first cell fate specification of the dividing mouse embryo, which results in the formation of the blastocyst. To address this issue directly, we generated zygotes in which both the maternal and the zygotic expression of Rbpsuh, a key element of the core Notch signaling pathway, were abrogated. We find that such zygotes give rise to blastocysts which implant and develop normally. Nevertheless, after gastrulation, these embryos die around midgestation, similarly to Rbpsuh-null mutants. This demonstrates that the RBP-Jκ-dependent pathway, otherwise called the canonical Notch pathway, is dispensable for blastocyst morphogenesis and the establishment of the three germ layers, ectoderm, endoderm, and mesoderm. These results are discussed in the light of recent observations which have challenged this conclusion.

scholarly journals Transgenic Expression of Numb Inhibits Notch Signaling in Immature Thymocytes But Does Not Alter T Cell Fate Specification

2002 ◽  
Vol 168 (7) ◽  
pp. 3173-3180 ◽  
Author(s):  
Michelle B. French ◽  
Ute Koch ◽  
Rachel E. Shaye ◽  
Melanie A. McGill ◽  
Sascha E. Dho ◽  
...  
Keyword(s):  
T Cell ◽  
Notch Signaling ◽  
Cell Fate ◽  
Cell Fate Specification ◽  
Transgenic Expression ◽  
Fate Specification ◽  
Immature Thymocytes

Glial cell fate specification modulated by the bHLH gene Hes5 in mouse retina

Development ◽  
2000 ◽  
Vol 127 (12) ◽  
pp. 2515-2522 ◽  
Author(s):  
M. Hojo ◽  
T. Ohtsuka ◽  
N. Hashimoto ◽  
G. Gradwohl ◽  
F. Guillemot ◽  
...  
Keyword(s):  
Glial Cell ◽  
Cell Fate ◽  
Glial Cells ◽  
Expression Patterns ◽  
Cell Number ◽  
Current Data ◽  
Mouse Retina ◽  
Cell Fate Specification ◽  
Bhlh Gene ◽  
Fate Specification

Neurons and glial cells differentiate from common precursors. Whereas the gene glial cells missing (gcm) determines the glial fate in Drosophila, current data about the expression patterns suggest that, in mammals, gcm homologues are unlikely to regulate gliogenesis. Here, we found that, in mouse retina, the bHLH gene Hes5 was specifically expressed by differentiating Muller glial cells and that misexpression of Hes5 with recombinant retrovirus significantly increased the population of glial cells at the expense of neurons. Conversely, Hes5-deficient retina showed 30–40% decrease of Muller glial cell number without affecting cell survival. These results indicate that Hes5 modulates glial cell fate specification in mouse retina.

scholarly journals KIF18B is a cell-type specific regulator of spindle orientation in the epidermis

2021 ◽  
pp. mbc.E21-06-0291
Author(s):  
Rebecca S. Moreci ◽  
Terry Lechler
Keyword(s):  
Cell Division ◽  
Hair Follicle ◽  
Cell Fate ◽  
Asymmetric Cell Division ◽  
Microtubule Dynamics ◽  
Spindle Orientation ◽  
Cell Cortex ◽  
Cell Fate Specification ◽  
Cell Fate Decisions ◽  
Fate Specification

Proper spindle orientation is required for asymmetric cell division and the establishment of complex tissue architecture. In the developing epidermis, spindle orientation requires a conserved cortical protein complex of LGN/NuMA/dynein-dynactin. However, how microtubule dynamics are regulated to interact with this machinery and properly position the mitotic spindle is not fully understood. Furthermore, our understanding of the processes that link spindle orientation during asymmetric cell division to cell fate specification in distinct tissue contexts remains incomplete. We report a role for the microtubule catastrophe factor KIF18B in regulating microtubule dynamics to promote spindle orientation in keratinocytes. During mitosis, KIF18B accumulates at the cell cortex, colocalizing with the conserved spindle orientation machinery. In vivo we find that KIF18B is required for oriented cell divisions within the hair placode, the first stage of hair follicle morphogenesis, but is not essential in the interfollicular epidermis. Disrupting spindle orientation in the placode, using mutations in either KIF18B or NuMA, results in aberrant cell fate marker expression of hair follicle progenitor cells. These data functionally link spindle orientation to cell fate decisions during hair follicle morphogenesis. Taken together, our data demonstrate a role for regulated microtubule dynamics in spindle orientation in epidermal cells. This work also highlights the importance of spindle orientation during asymmetric cell division to dictate cell fate specification. [Media: see text] [Media: see text]

scholarly journals Multimodal Long Noncoding RNA Interaction Networks: Control Panels for Cell Fate Specification

Genetics ◽  
2019 ◽  
Vol 213 (4) ◽  
pp. 1093-1110 ◽  
Author(s):  
Keriayn N. Smith ◽  
Sarah C. Miller ◽  
Gabriele Varani ◽  
J. Mauro Calabrese ◽  
Terry Magnuson
Keyword(s):  
Cell Fate ◽  
Early Development ◽  
Noncoding Rna ◽  
Cell Types ◽  
Cell Fate Specification ◽  
Phenotypic Analysis ◽  
Cell Fate Decisions ◽  
Fate Specification ◽  
Mechanistic Basis ◽  
Rna Interaction

Lineage specification in early development is the basis for the exquisitely precise body plan of multicellular organisms. It is therefore critical to understand cell fate decisions in early development. Moreover, for regenerative medicine, the accurate specification of cell types to replace damaged/diseased tissue is strongly dependent on identifying determinants of cell identity. Long noncoding RNAs (lncRNAs) have been shown to regulate cellular plasticity, including pluripotency establishment and maintenance, differentiation and development, yet broad phenotypic analysis and the mechanistic basis of their function remains lacking. As components of molecular condensates, lncRNAs interact with almost all classes of cellular biomolecules, including proteins, DNA, mRNAs, and microRNAs. With functions ranging from controlling alternative splicing of mRNAs, to providing scaffolding upon which chromatin modifiers are assembled, it is clear that at least a subset of lncRNAs are far from the transcriptional noise they were once deemed. This review highlights the diversity of lncRNA interactions in the context of cell fate specification, and provides examples of each type of interaction in relevant developmental contexts. Also highlighted are experimental and computational approaches to study lncRNAs.

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