Synthesis and content of DNA in epidermal cell nuclei of mouse skin during differentiation and specialization

Каралова, Е М; Petrosyan, Agavni; Abroyan, Liana; Nozdrin, V. I.; Magakyan, Yu. A.

doi:10.1007/bf00840861

Cited by 4 publications

(4 citation statements)

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“…S3b,c; 18,77,78). Consistently, increased nuclear size in suprabasal cells has also been reported (Table 1; 18,77,79). Our estimations are that the polyploid proportion of cells within differentiating epidermis of normal skin, at a given time, may be around 50-60% (tetraploids 1 While cells in G0 can increase in size, this capacity is limited compared with the large size resulting from successive cell cycles of growth in the absence of cell division.…”

Section: The Evidencesupporting

confidence: 86%

Cycling up the epidermis: reconciling 100 years of debate

Gandarillas

Freije

2013

Experimental Dermatology

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There is likely general consensus within the skin research community that cell cycle control is critical to epidermal homeostasis and disease. The current predominant model proposes that keratinocytes switch off DNA replication and undergo cell cycle and cell growth arrest as they initiate terminal differentiation. However, this model cannot explain key physiological features of the skin, mainly why squamous differentiation prevails over proliferation in benign hyperproliferative disorders. In recent years, we have proposed an alternative model that involves mitotic slippage and endoreplication. This new model is controversial and has encountered resistance within the field. However, looking back at history, the epidermal cell cycle has been a matter of controversy and debate for around 100 years now. The accumulated data are confusing and contradictory. Our present model can explain and reconcile both old and new paradoxical observations. Here, we explain and discuss the endoreplicative cell cycle, the evidence for and against its existence in human epidermis and the important implications for skin homeostasis and disease. We show that regardless of the strengths or weaknesses of the Endoreplication Model, the existing evidence in support of the Cell Cycle Arrest Model is very weak.

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Section: The Evidencesupporting

confidence: 86%

Cycling up the epidermis: reconciling 100 years of debate

Gandarillas

Freije

2013

Experimental Dermatology

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“…Using fluorescence in situ hybridization (FISH) assays, we confirmed the presence of some polyploid cells in the suprabasal layers of mouse skin ( Fig. 3 A), in agreement with previous observations ( Karalova et al, 1988 ; Kartasova et al, 1992 ). In light of these findings and that a mitotic arrest (e.g.…”

Section: Resultssupporting

confidence: 91%

Clasp2 ensures mitotic fidelity and prevents differentiation of epidermal keratinocytes

Shahbazi

Peña-Jiménez

Antonucci

et al. 2017

Journal of Cell Science

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Epidermal homeostasis is tightly controlled by a balancing act of self-renewal or terminal differentiation of proliferating basal keratinocytes. An increase in DNA content as a consequence of a mitotic block is a recognized mechanism underlying keratinocyte differentiation, but the molecular mechanisms involved in this process are not yet fully understood. Using cultured primary keratinocytes, here we report that the expression of the mammalian microtubule and kinetochore-associated protein Clasp2 is intimately associated with the basal proliferative makeup of keratinocytes, and its deficiency leads to premature differentiation. Clasp2-deficient keratinocytes exhibit increased centrosomal numbers and numerous mitotic alterations, including multipolar spindles and chromosomal misalignments that overall result in mitotic stress and a high DNA content. Such mitotic block prompts premature keratinocyte differentiation in a p53-dependent manner in the absence of cell death. Our findings reveal a new role for Clasp2 in governing keratinocyte undifferentiated features and highlight the presence of surveillance mechanisms that prevent cell cycle entry in cells that have alterations in the DNA content.

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“…Using fluorescence in situ hybridization (FISH) assays, we confirmed the presence of some polyploid cells in the suprabasal layers of mouse skin (Fig. 3A), in agreement with previous observations (Karalova et al, 1988;Kartasova et al, 1992). In light of these findings and that a mitotic arrest (e.g.…”

Section: Clasp2 Expression Ensures Mitotic Fidelity In Primary Mouse supporting

confidence: 91%

Clasp2 ensures mitotic fidelity and prevents differentiation of epidermal keratinocytes

Shahbazi¹,

Peña-Jiménez²,

Antonucci³

et al. 2017

Development

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Epidermal homeostasis is tightly controlled by a balancing act of selfrenewal or terminal differentiation of proliferating basal keratinocytes. An increase in DNA content as a consequence of a mitotic block is a recognized mechanism underlying keratinocyte differentiation, but the molecular mechanisms involved in this process are not yet fully understood. Using cultured primary keratinocytes, here we report that the expression of the mammalian microtubule and kinetochoreassociated protein Clasp2 is intimately associated with the basal proliferative makeup of keratinocytes, and its deficiency leads to premature differentiation. Clasp2-deficient keratinocytes exhibit increased centrosomal numbers and numerous mitotic alterations, including multipolar spindles and chromosomal misalignments that overall result in mitotic stress and a high DNA content. Such mitotic block prompts premature keratinocyte differentiation in a p53-dependent manner in the absence of cell death. Our findings reveal a new role for Clasp2 in governing keratinocyte undifferentiated features and highlight the presence of surveillance mechanisms that prevent cell cycle entry in cells that have alterations in the DNA content.

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Synthesis and content of DNA in epidermal cell nuclei of mouse skin during differentiation and specialization

Cited by 4 publications

References 1 publication

Cycling up the epidermis: reconciling 100 years of debate

Cycling up the epidermis: reconciling 100 years of debate

Clasp2 ensures mitotic fidelity and prevents differentiation of epidermal keratinocytes

Clasp2 ensures mitotic fidelity and prevents differentiation of epidermal keratinocytes

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