scholarly journals Fgf8 induces pillar cell fate and regulates cellular patterning in the mammalian cochlea

Development ◽  
2007 ◽  
Vol 134 (16) ◽  
pp. 3021-3029 ◽  
Author(s):  
B. E. Jacques ◽  
M. E. Montcouquiol ◽  
E. M. Layman ◽  
M. Lewandoski ◽  
M. W. Kelley

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 606 ◽  
Author(s):  
Konrad Winnicki

In plants, the first asymmetrical division of a zygote leads to the formation of two cells with different developmental fates. The establishment of various patterns relies on spatial and temporal gene expression, however the precise mechanism responsible for embryonic patterning still needs elucidation. Auxin seems to be the main player which regulates embryo development and controls expression of various genes in a dose-dependent manner. Thus, local auxin maxima and minima which are provided by polar auxin transport underlie cell fate specification. Diverse auxin concentrations in various regions of an embryo would easily explain distinct cell identities, however the question about the mechanism of cellular patterning in cells exposed to similar auxin concentrations still remains open. Thus, specification of cell fate might result not only from the cell position within an embryo but also from events occurring before and during mitosis. This review presents the impact of auxin on the orientation of the cell division plane and discusses the mechanism of auxin-dependent cytoskeleton alignment. Furthermore, close attention is paid to auxin-induced calcium fluxes, which regulate the activity of MAPKs during postembryonic development and which possibly might also underlie cellular patterning during embryogenesis.



2009 ◽  
Vol 16 (1) ◽  
pp. 58-69 ◽  
Author(s):  
Angelika Doetzlhofer ◽  
Martin L. Basch ◽  
Takahiro Ohyama ◽  
Manfred Gessler ◽  
Andrew K. Groves ◽  
...  


2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.



2020 ◽  
Vol 64 (2) ◽  
pp. 223-232 ◽  
Author(s):  
Ben L. Carty ◽  
Elaine M. Dunleavy

Abstract Asymmetric cell division (ACD) produces daughter cells with separate distinct cell fates and is critical for the development and regulation of multicellular organisms. Epigenetic mechanisms are key players in cell fate determination. Centromeres, epigenetically specified loci defined by the presence of the histone H3-variant, centromere protein A (CENP-A), are essential for chromosome segregation at cell division. ACDs in stem cells and in oocyte meiosis have been proposed to be reliant on centromere integrity for the regulation of the non-random segregation of chromosomes. It has recently been shown that CENP-A is asymmetrically distributed between the centromeres of sister chromatids in male and female Drosophila germline stem cells (GSCs), with more CENP-A on sister chromatids to be segregated to the GSC. This imbalance in centromere strength correlates with the temporal and asymmetric assembly of the mitotic spindle and potentially orientates the cell to allow for biased sister chromatid retention in stem cells. In this essay, we discuss the recent evidence for asymmetric sister centromeres in stem cells. Thereafter, we discuss mechanistic avenues to establish this sister centromere asymmetry and how it ultimately might influence cell fate.



2014 ◽  
Author(s):  
Patrick Seale ◽  
Wenshan Wang ◽  
Sona Rajakumari ◽  
Matthew Harms


2003 ◽  
Vol 773 ◽  
Author(s):  
James D. Kubicek ◽  
Stephanie Brelsford ◽  
Philip R. LeDuc

AbstractMechanical stimulation of single cells has been shown to affect cellular behavior from the molecular scale to ultimate cell fate including apoptosis and proliferation. In this, the ability to control the spatiotemporal application of force on cells through their extracellular matrix connections is critical to understand the cellular response of mechanotransduction. Here, we develop and utilize a novel pressure-driven equibiaxial cell stretching device (PECS) combined with an elastomeric material to control specifically the mechanical stimulation on single cells. Cells were cultured on silicone membranes coated with molecular matrices and then a uniform pressure was introduced to the opposite surface of the membrane to stretch single cells equibiaxially. This allowed us to apply mechanical deformation to investigate the complex nature of cell shape and structure. These results will enhance our knowledge of cellular and molecular function as well as provide insights into fields including biomechanics, tissue engineering, and drug discovery.



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