scholarly journals Lamin complexes in the nuclear interior control progenitor cell proliferation and tissue homeostasis

Cell Cycle ◽  
2009 ◽  
Vol 8 (10) ◽  
pp. 1488-1493 ◽  
Author(s):  
Nana Naetar ◽  
Roland Foisner
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cell ◽  
Tissue Homeostasis ◽  
Nuclear Interior ◽  
Progenitor Cell Proliferation

scholarly journals Regulated spindle orientation buffers tissue growth in the epidermis

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Angel Morrow ◽  
Julie Underwood ◽  
Lindsey Seldin ◽  
Taylor Hinnant ◽  
Terry Lechler
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cell ◽  
Tissue Growth ◽  
Tissue Homeostasis ◽  
Tissue Loss ◽  
Spindle Orientation ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions ◽  
Mammalian Skin ◽  
Progenitor Cell Proliferation

Tissue homeostasis requires a balance between progenitor cell proliferation and loss. Mechanisms that maintain this robust balance are needed to avoid tissue loss or overgrowth. Here we demonstrate that regulation of spindle orientation/asymmetric cell divisions is one mechanism that is used to buffer changes in proliferation and tissue turnover in mammalian skin. Genetic and pharmacologic experiments demonstrate that asymmetric cell divisions were increased in hyperproliferative conditions and decreased under hypoproliferative conditions. Further, active K-Ras also increased the frequency of asymmetric cell divisions. Disruption of spindle orientation in combination with constitutively active K-Ras resulted in massive tissue overgrowth. Together, these data highlight the essential roles of spindle orientation in buffering tissue homeostasis in response to perturbations.

scholarly journals Regulated spindle orientation buffers tissue growth in the epidermis

2019 ◽  
Author(s):  
Angel Morrow ◽  
Julie Underwood ◽  
Lindsey Seldin ◽  
Taylor Hinnant ◽  
Terry Lechler
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cell ◽  
Tissue Growth ◽  
Tissue Homeostasis ◽  
Tissue Loss ◽  
Spindle Orientation ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions ◽  
Mammalian Skin ◽  
Progenitor Cell Proliferation

SummaryTissue homeostasis requires a balance between progenitor cell proliferation and loss. Mechanisms that maintain this robust balance are needed to avoid tissue loss or overgrowth. Here we demonstrate that regulation of spindle orientation/asymmetric cell divisions is one mechanism that is used to buffer changes in proliferation and tissue turnover in mammalian skin. Genetic and pharmacologic experiments demonstrate that asymmetric cell divisions were increased in hyperproliferative conditions and decreased under hypoproliferative conditions. Further, active K-Ras also increased the frequency of asymmetric cell divisions. Disruption of spindle orientation in combination with constitutively active K-Ras resulted in massive tissue overgrowth. Together, these data highlight the essential roles of spindle orientation in buffering tissue homeostasis in response to perturbations.

scholarly journals Histone chaperone HIRA regulates neural progenitor cell proliferation and neurogenesis via β-catenin

2017 ◽  
Vol 216 (7) ◽  
pp. 1975-1992 ◽  
Author(s):  
Yanxin Li ◽  
Jianwei Jiao
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Progenitor Cell ◽  
Neural Progenitor Cells ◽  
Neural Progenitor Cell ◽  
Neural Progenitor ◽  
Histone Chaperone ◽  
Epigenetic Mechanism ◽  
Progenitor Cell Proliferation ◽  
Early Neurogenesis

Histone cell cycle regulator (HIRA) is a histone chaperone and has been identified as an epigenetic regulator. Subsequent studies have provided evidence that HIRA plays key roles in embryonic development, but its function during early neurogenesis remains unknown. Here, we demonstrate that HIRA is enriched in neural progenitor cells, and HIRA knockdown reduces neural progenitor cell proliferation, increases terminal mitosis and cell cycle exit, and ultimately results in premature neuronal differentiation. Additionally, we demonstrate that HIRA enhances β-catenin expression by recruiting H3K4 trimethyltransferase Setd1A, which increases H3K4me3 levels and heightens the promoter activity of β-catenin. Significantly, overexpression of HIRA, HIRA N-terminal domain, or β-catenin can override neurogenesis abnormities caused by HIRA defects. Collectively, these data implicate that HIRA, cooperating with Setd1A, modulates β-catenin expression and then regulates neurogenesis. This finding represents a novel epigenetic mechanism underlying the histone code and has profound and lasting implications for diseases and neurobiology.

scholarly journals The cell biology of regeneration

2012 ◽  
Vol 196 (5) ◽  
pp. 553-562 ◽  
Author(s):  
Ryan S. King ◽  
Phillip A. Newmark
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Biology ◽  
Progenitor Cell ◽  
Complex Structures ◽  
Regenerative Processes ◽  
Cellular Behavior ◽  
Positional Identity ◽  
Progenitor Cell Proliferation ◽  
Functional Analyses

Regeneration of complex structures after injury requires dramatic changes in cellular behavior. Regenerating tissues initiate a program that includes diverse processes such as wound healing, cell death, dedifferentiation, and stem (or progenitor) cell proliferation; furthermore, newly regenerated tissues must integrate polarity and positional identity cues with preexisting body structures. Gene knockdown approaches and transgenesis-based lineage and functional analyses have been instrumental in deciphering various aspects of regenerative processes in diverse animal models for studying regeneration.

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