scholarly journals Intrinsic Cell Polarity Coupled to Growth Axis Formation in Tobacco BY-2 Cells

2020 ◽  
Vol 30 (24) ◽  
pp. 4999-5006.e3
Author(s):  
Jordi Chan ◽  
Catherine Mansfield ◽  
Flavie Clouet ◽  
Delfi Dorussen ◽  
Enrico Coen
Development ◽  
2001 ◽  
Vol 128 (5) ◽  
pp. 665-673 ◽  
Author(s):  
N. MacDougall ◽  
Y. Lad ◽  
G.S. Wilkie ◽  
H. Francis-Lang ◽  
W. Sullivan ◽  
...  

In Drosophila, the formation of the embryonic axes is initiated by Gurken, a transforming growth factor alpha signal from the oocyte to the posterior follicle cells, and an unknown polarising signal back to the oocyte. We report that Drosophila Merlin is specifically required only within the posterior follicle cells to initiate axis formation. Merlin mutants show defects in nuclear migration and mRNA localisation in the oocyte. Merlin is not required to specify posterior follicle cell identity in response to the Gurken signal from the oocyte, but is required for the unknown polarising signal back to the oocyte. Merlin is also required non-autonomously, only in follicle cells that have received the Gurken signal, to maintain cell polarity and limit proliferation, but is not required in embryos and larvae. These results are consistent with the fact that human Merlin is encoded by the gene for the tumour suppressor neurofibromatosis-2 and is a member of the Ezrin-Radixin-Moesin family of proteins that link actin to transmembrane proteins. We propose that Merlin acts in response to the Gurken signal by apically targeting the signal that initiates axis specification in the oocyte.


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.


2021 ◽  
Vol 67 (1 Jan-Feb) ◽  
pp. 7
Author(s):  
B. Bachir Bouiadjra ◽  
N. Mehnane ◽  
N. Oukli

Based on the full potential linear muffin-tin orbitals (FPLMTO) calculation within density functional theory, we systematically investigate the electronic and optical properties of (100) and (110)-oriented (InN)/(GaN)n zinc-blende superlattice with one InN monolayer and with different numbers of GaN monolayers. Specifically, the electronic band structure calculations and their related features, like the absorption coefficient and refractive index of these systems are computed over a wide photon energy scale up to 20 eV. The effect of periodicity layer numbers n on the band gaps and the optical activity of (InN)/(GaN)n SLs in the both  growth axis (001) and (110) are examined and compared. Because of prospective optical aspects of (InN)/(GaN)n such as light-emitting applications, this theoretical study can help the experimental measurements.


Author(s):  
Daniel Nuez ◽  
Phoumra Tan

Abstract Conductive anodic filament (CAF) formation is a mechanism caused by an electrochemical migration of metals from a metal trace in ICs or in PCBs. This is commonly caused by the moisture build-up in the affected metal terminals in an IC package or PC board caused by critical temperature, high humidity and high voltage gradients conditions. This phenomenon is known to have caused catastrophic field failures on various OEMs electronic components in the past [1,7]. Most published articles on CAF described the formation of the filament in a lateral formation through the glass fiber interfaces between two adjacent metal planes [1-6, 8-12]. One common example is the CAF formation seen between PTH (Plated through Hole) in the laminated substrate with two different potentials causing shorts [1-6, 8-12]. In this paper, the Cu filament grows in a vertical fashion (z-axis formation) creating a vertical plane shorts between the upper and lower metal terminals in a laminated IC package substrate. The copper growth migration does not follow the fiber strands laterally or vertically through them. Instead, it grows through the stress created gaps between the impregnated carbon epoxy fillers from the upper metal trace to the lower metal trace with two different potentials, between the glass fibers. This vertical CAF mechanism creates a low resistive short that was sometimes found to be intermittent in nature. This paper presents some successful failure analysis approaches used to isolate and detect the failure locations for this type of failing devices. This paper also exposes the unique physical appearance of the vertical CAF formation.


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