scholarly journals Secondary loss of miR-3607 reduced cortical progenitor amplification during rodent evolution

2022 ◽  
Vol 8 (2) ◽  
Author(s):  
Kaviya Chinnappa ◽  
Adrián Cárdenas ◽  
Anna Prieto-Colomina ◽  
Ana Villalba ◽  
Ángel Márquez-Galera ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cerebral Cortex ◽  
Progenitor Cell ◽  
Secondary Loss ◽  
Progenitor Cell Proliferation ◽  
Cortical Progenitor

Expression of miR-3607 in embryonic mammalian cerebral cortex was lost in rodents, limiting progenitor cell proliferation.

scholarly journals The Extracellular Matrix in the Evolution of Cortical Development and Folding

2020 ◽  
Vol 8 ◽  
Author(s):  
Salma Amin ◽  
Víctor Borrell
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Cerebral Cortex ◽  
Neuronal Migration ◽  
Progenitor Cell ◽  
Expression Profiles ◽  
Functional Studies ◽  
Structural Framework ◽  
Neocortical Development ◽  
Progenitor Cell Proliferation

The evolution of the mammalian cerebral cortex leading to humans involved a remarkable sophistication of developmental mechanisms. Specific adaptations of progenitor cell proliferation and neuronal migration mechanisms have been proposed to play major roles in this evolution of neocortical development. One of the central elements influencing neocortex development is the extracellular matrix (ECM). The ECM provides both a structural framework during tissue formation and to present signaling molecules to cells, which directly influences cell behavior and movement. Here we review recent advances in the understanding of the role of ECM molecules on progenitor cell proliferation and neuronal migration, and how these contribute to cerebral cortex expansion and folding. We discuss how transcriptomic studies in human, ferret and mouse identify components of ECM as being candidate key players in cortex expansion during development and evolution. Then we focus on recent functional studies showing that ECM components regulate cortical progenitor cell proliferation, neuron migration and the mechanical properties of the developing cortex. Finally, we discuss how these features differ between lissencephalic and gyrencephalic species, and how the molecular evolution of ECM components and their expression profiles may have been fundamental in the emergence and evolution of cortex folding across mammalian phylogeny.

Contact-mediated inhibition of human haematopoietic progenitor cell proliferation may be conferred by stem cell antigen, CD34

2000 ◽  
Vol 1 (2) ◽  
pp. 77-86 ◽  
Author(s):  
M Y Gordon ◽  
S B Marley ◽  
R J Davidson ◽  
F H Grand ◽  
J L Lewis ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Progenitor Cell ◽  
Haematopoietic Progenitor Cell ◽  
Cell Antigen ◽  
Progenitor Cell Proliferation

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.

Sign in / Sign up

Export Citation Format

Share Document