Epiboly generates the epidermal basal monolayer and spreads the nascent mammalian skin to enclose the embryonic body

Panousopoulou, Eleni; Hobbs, Carl; Mason, Ivor; Green, Jeremy; Formstone, Caroline J.

doi:10.1242/dev.139352

Cited by 4 publications

(4 citation statements)

References 52 publications

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“…Epiboly is a basic developmental process during which the area of a cell sheet is increased by radial intercalation (16,17). Epiboly also occurs in developing skin (24). These examples include not only isotropically but also anisotropically expanding fields; however, the volume increase in embryonic cavities and epiboly can provide almost isotropic expansion of fields.…”

Section: Discussionmentioning

confidence: 99%

Isotropic expansion of external environment induces tissue elongation and collective cell alignment

Koyama

Fujimori

2020

Journal of Theoretical Biology

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Cell movement is crucial for morphogenesis in multicellular organisms. Growing embryos or tissues often expand isotropically, i.e., uniformly, in all dimensions. On the surfaces of these expanding environments, which we call "fields," cells are subjected to frictional forces and move passively in response. However, the potential roles of isotropically expanding fields in morphogenetic events have not been investigated well.In this study, we mathematically analyzed the effect of isotropically expanding fields using a vertex model, a standard type of multi-cellular model. We found that cells located on fields were elongated along a similar direction each other. Simultaneously, the cell clusters were also elongated, even though field expansion was absolutely isotropic. We then investigated the mechanism underlying these counterintuitive phenomena. In particular, we asked whether elongation was caused by the properties of the field, the cell cluster, or both. Theoretical analyses involving simplification of the model revealed that cell clusters have an intrinsic ability to asymmetrically deform, leading to their elongation. Importantly, this ability is effective only under the non-equilibrium conditions provided by field expansion. This may explain the elongation of the notochord, located on the surface of the growing mouse embryo. We established that passive cell movement induced by isotropically expanding external

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Section: Discussionmentioning

confidence: 99%

Isotropic expansion of external environment induces tissue elongation and collective cell alignment

Koyama

Fujimori

2020

Journal of Theoretical Biology

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“…bs‐4592R, Bioss, 1:100 dilution) antibodies or the sections were HE stained. Epidermal thickness was measured as described by Eleni Panousopoulou et al 27 In brief, the depth of the epidermis was measured using the ruler tool and converted with reference to the scale bar in the software Volocity. Image‐Pro Plus 6.0 was used to score the integrated optical density (IOD) as a measure of the HREC3 expression in the skin and to count the number of p16‐positive cells 28 .…”

Section: Methodsmentioning

confidence: 99%

Ultraviolet B irradiation up‐regulates MM1 and induces photoageing of the epidermis

Zheng

Chen

Jin

et al. 2021

Photoderm Photoimm Photomed

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Background: ΔNp63α and c-Myc are key transcription factors controlling proliferation and senescence in epithelial cells. We previously reported that the c-Myc modulator MM1 and its E3 ligase, HERC3, together with the transcription factor ΔNp63α, compose a feedback loop, which regulates proliferative senescence in MCF-10A mammary epithelial cells. However, it is unknown whether this loop is involved in skin ageing. On the other hand, ultraviolet B (UVB) rays are assumed to be the main culprits for photoageing of the epidermis, but the underlying mechanisms are obscure.Aims: To investigate whether MM1/ΔNp63α axis is involved in UVB-induced photoageing of the epidermis. Materials and Methods:HaCaT human immortalized keratinocytes overexpressed with MM1, knocked down with c-Myc or irradiated with UVB, were subjected to MTT assays to measure cell proliferation, as well as RT-qPCR or immunoblot to detect the members of MM1/ΔNp63α loop and the cellular senescence markers. Meanwhile, primary normal human keratinocytes (NHKs) or mice were irradiated with UVB, followed by immunoblot analysis, SAβ-gal, haematoxylin-eosin or immunohistochemistry staining. Results: Overexpression of MM1 down-regulated ΔNp63α and induced proliferative senescence in the HaCaT cells. In the HaCaT cells, NHKs and the mouse epidermis, UVB irradiation increased MM1 mRNA level and led to a down-regulation of ΔNp63α, HERC3 and c-Myc, concomitant with cellular senescence or photoageing. Additionally, knock-down of c-Myc induced proliferative senescence in the HaCaT cells and abrogated UVB-induced cellular senescence. Conclusions: UVB up-regulates MM1 and consequently modulates ΔNp63α and c-Myc, which may account for the proliferative senescence of keratinocytes and photoageing of the epidermis.

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“…The planar cell polarity cadherin receptor CELSR1 has been shown to regulate mouse skin hair patterning in a similar way to frizzled receptor 6 (FZD6), indicating that both GPCRs participate in the same developmental polarity pathway 108,109 (Figure 4C). CELSR1 has also been involved in the process of epidermal cell spreading during mouse development 110 . ADGRF2 (GPR111) and ADGRF4 (GPR115) expression are particularly enriched in mouse epidermis, although single knockout for these individual GPCRs has no effect in skin 111 …”

Section: Gpcrs Involved In the Regulation Of Skin Biologymentioning

confidence: 99%

The landscape of GPCR signaling in the regulation of epidermal stem cell fate and skin homeostasis

2020

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Continuous integration of signals from the micro- and macro-environment is necessary for somatic stem cells to adapt to changing conditions, maintain tissue homeostasis, and activate repair mechanisms. G-protein coupled receptors (GPCRs) facilitate this integration by binding to numerous hormones, metabolites, and inflammatory mediators, influencing a diverse network of pathways that regulate stem cell fate. This adaptive mechanism is particularly relevant for tissues that are exposed to environmental assault, like skin. The skin is maintained by a set of basal keratinocyte stem and progenitor cells located in the hair follicle and interfollicular epidermis, and several GPCRs and their signaling partners serve as makers and regulators of epidermal stem cell activity. GPCRs utilize heterotrimeric G protein dependent and independent pathways to translate extracellular signals into intracellular molecular cascades that dictate the activation of keratinocyte proliferative and differentiation networks, including Hedgehog GLI, Hippo YAP1 and WNT/β-catenin, ultimately regulating stem cell identity. Dysregulation of GPCR signaling underlines numerous skin inflammatory diseases and cancer, with smoothened-driven basal cell carcinoma being a main example of a GPCR-associated cancer. In this review, we discuss the impact of GPCRs and their signaling partners in skin keratinocyte biology, particularly in the regulation of the epidermal stem cell compartment.

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Epiboly generates the epidermal basal monolayer and spreads the nascent mammalian skin to enclose the embryonic body

Cited by 4 publications

References 52 publications

Isotropic expansion of external environment induces tissue elongation and collective cell alignment

Isotropic expansion of external environment induces tissue elongation and collective cell alignment

Ultraviolet B irradiation up‐regulates MM1 and induces photoageing of the epidermis

The landscape of GPCR signaling in the regulation of epidermal stem cell fate and skin homeostasis

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