scholarly journals Polar cell fate stimulatesWolbachiaintracellular growth

Development ◽  
2018 ◽  
Vol 145 (6) ◽  
pp. dev158097 ◽  
Author(s):  
Ajit D. Kamath ◽  
Mark A. Deehan ◽  
Horacio M. Frydman
Keyword(s):  
Cell Fate ◽  
Polar Cell

fringeandNotchspecify polar cell fate duringDrosophilaoogenesis

Development ◽  
2001 ◽  
Vol 128 (12) ◽  
pp. 2243-2253 ◽  
Author(s):  
Muriel Grammont ◽  
Kenneth D. Irvine
Keyword(s):  
Cell Fate ◽  
Null Allele ◽  
Somatic Cells ◽  
Ectopic Expression ◽  
Notch Receptor ◽  
Drosophila Oogenesis ◽  
Early Stages ◽  
Polar Cell ◽  
Hypomorphic Alleles ◽  
Notch Activation

fringe encodes a glycosyltransferase that modulates the ability of the Notch receptor to be activated by its ligands. We describe studies of fringe function during early stages of Drosophila oogenesis. Animals mutant for hypomorphic alleles of fringe contain follicles with an incorrect number of germline cells, which are separated by abnormally long and disorganized stalks. Analysis of clones of somatic cells mutant for a null allele of fringe localizes the requirement for fringe in follicle formation to the polar cells, and demonstrates that fringe is required for polar cell fate. Clones of cells mutant for Notch also lack polar cells and the requirement for Notch in follicle formation appears to map to the polar cells. Ectopic expression of fringe or of an activated form of Notch can generate an extra polar cell. Our results indicate that fringe plays a key role in positioning Notch activation during early oogenesis, and establish a function for the polar cells in separating germline cysts into individual follicles.

Decoding vectorial information from a gradient: sequential roles of the receptors Frizzled and Notch in establishing planar polarity in the Drosophila eye

Development ◽  
1999 ◽  
Vol 126 (24) ◽  
pp. 5725-5738 ◽  
Author(s):  
A. Tomlinson ◽  
G. Struhl
Keyword(s):  
High Activity ◽  
Cell Fate ◽  
Photoreceptor Cells ◽  
The Other ◽  
Cell Fate Decision ◽  
Planar Polarity ◽  
Genetic Mosaics ◽  
Polar Cell ◽  
Drosophila Eye ◽  
Fate Decision

The Drosophila eye is composed of several hundred ommatidia that can exist in either of two chiral forms, depending on position: ommatidia in the dorsal half of the eye adopt one chiral form, whereas ommatidia in the ventral half adopt the other. Chirality appears to be specified by a polarizing signal with a high activity at the interface between the two halves (the ‘equator’), which declines in opposite directions towards the dorsal and ventral poles. Here, using genetic mosaics, we show that this polarizing signal is decoded by the sequential use of two receptor systems. The first depends on the seven-transmembrane receptor Frizzled (Fz) and distinguishes between the two members of the R3/R4 pair of presumptive photoreceptor cells, predisposing the cell that is located closer to the equator and having higher Fz activity towards the R3 photoreceptor fate and the cell further away towards the R4 fate. This bias is then amplified by subsequent interactions between the two cells mediated by the receptor Notch (N) and its ligand Delta (Dl), ensuring that the equatorial cell becomes the R3 photoreceptor while the polar cell becomes the R4 photoreceptor. As a consequence of this reciprocal cell fate decision, the R4 cell moves asymmetrically relative to the R3 cell, initiating the appropriate chiral pattern of the remaining cells of the ommatidium.

scholarly journals The Hippo pathway controls polar cell fate through Notch signaling during Drosophila oogenesis

2011 ◽  
Vol 357 (2) ◽  
pp. 370-379 ◽  
Author(s):  
Hsi-Ju Chen ◽  
Chi-Ming Wang ◽  
Tsu-Wei Wang ◽  
Gwo-Jen Liaw ◽  
Ta-Hsing Hsu ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Hippo Pathway ◽  
Drosophila Oogenesis ◽  
Polar Cell ◽  
The Hippo Pathway

Mosaic Analysis in the Drosophila Ovary Reveals a Common Hedgehog-Inducible Precursor Stage for Stalk and Polar Cells

Genetics ◽  
1999 ◽  
Vol 151 (2) ◽  
pp. 739-748 ◽  
Author(s):  
Michael Tworoger ◽  
Michele Keller Larkin ◽  
Zev Bryant ◽  
Hannele Ruohola-Baker
Keyword(s):  
Cell Fate ◽  
Ovarian Follicle ◽  
Ectopic Expression ◽  
Cell Formation ◽  
Follicle Cells ◽  
Stalk Cell ◽  
Polar Cell ◽  
Drosophila Ovary ◽  
Anterior Posterior

Abstract The fates of two small subgroups of the ovarian follicle cells appear to be linked: mutations in Notch, Delta, fs(1)Yb, or hedgehog cause simultaneous defects in the specification of stalk cells and polar cells. Both of these subgroups are determined in the germarium, and both cease division early in oogenesis. To test the possibility that these subgroups are related by lineage, we generated dominantly marked mitotic clones in ovaries. Small, restricted clones in stalk cells and polar cells were found adjacent to each other at a frequency much too high to be explained by independent induction. We therefore propose a model in which stalk cells and polar cells are derived from a precursor population that is distinct from the precursors for other follicle cells. We support and extend this model by characterization of mutants that affect stalk and polar cell formation. We find that ectopic expression of Hedgehog can induce both polar and stalk cell fate, presumably by acting on the precursor stage. In contrast, we find that stall affects neither the induction of the precursors nor the decision between the stalk cell and polar cell fate but, rather, some later differentiation step of stalk cells. In addition, we show that ectopic polar and stalk cells disturb the anterior-posterior polarity of the underlying oocyte.

Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Symmetry Breaking ◽  
Cell Fate ◽  
Cell Cortex ◽  
Axis Formation ◽  
Aurora A Kinase ◽  
Aurora A ◽  
C Elegans ◽  
Cell Embryo ◽  
Polarity Establishment

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.

Centromere assembly and non-random sister chromatid segregation in stem cells

2020 ◽  
Vol 64 (2) ◽  
pp. 223-232 ◽  
Author(s):  
Ben L. Carty ◽  
Elaine M. Dunleavy
Keyword(s):  
Stem Cells ◽  
Cell Division ◽  
Cell Fate ◽  
Sister Chromatid ◽  
Asymmetric Cell Division ◽  
Protein A ◽  
Germline Stem Cells ◽  
Sister Chromatids ◽  
Centromere Protein A ◽  
Oocyte Meiosis

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.

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