scholarly journals Cis-regulatory analysis of nodal and maternal control of dorsal-ventral axis formation by Univin, a TGF-  related to Vg1

Development ◽  
2007 ◽  
Vol 134 (20) ◽  
pp. 3649-3664 ◽  
Author(s):  
R. Range ◽  
F. Lapraz ◽  
M. Quirin ◽  
S. Marro ◽  
L. Besnardeau ◽  
...  
Keyword(s):  
Axis Formation ◽  
Maternal Control ◽  
Regulatory Analysis

scholarly journals An essential role for maternal control of Nodal signaling

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Pooja Kumari ◽  
Patrick C Gilligan ◽  
Shimin Lim ◽  
Long Duc Tran ◽  
Sylke Winkler ◽  
...  
Keyword(s):  
Untranslated Region ◽  
Sea Urchins ◽  
Axis Formation ◽  
Growth Factor Signaling ◽  
Nodal Signaling ◽  
New Paradigm ◽  
Maternal Control ◽  
Proteomic Screen ◽  
Maternal Transcripts ◽  
Stem Cell Pluripotency

Growth factor signaling is essential for pattern formation, growth, differentiation, and maintenance of stem cell pluripotency. Nodal-related signaling factors are required for axis formation and germ layer specification from sea urchins to mammals. Maternal transcripts of the zebrafish Nodal factor, Squint (Sqt), are localized to future embryonic dorsal. The mechanisms by which maternal sqt/nodal RNA is localized and regulated have been unclear. Here, we show that maternal control of Nodal signaling via the conserved Y box-binding protein 1 (Ybx1) is essential. We identified Ybx1 via a proteomic screen. Ybx1 recognizes the 3’ untranslated region (UTR) of sqt RNA and prevents premature translation and Sqt/Nodal signaling. Maternal-effect mutations in zebrafish ybx1 lead to deregulated Nodal signaling, gastrulation failure, and embryonic lethality. Implanted Nodal-coated beads phenocopy ybx1 mutant defects. Thus, Ybx1 prevents ectopic Nodal activity, revealing a new paradigm in the regulation of Nodal signaling, which is likely to be conserved.

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.

Failure Localization of Intermittent Short Failures Caused by Vertical Conductive Anodic Filament Formation

2014 ◽  
Author(s):  
Daniel Nuez ◽  
Phoumra Tan
Keyword(s):  
Glass Fibers ◽  
Vertical Plane ◽  
Axis Formation ◽  
Metal Trace ◽  
Conductive Anodic Filament ◽  
Plated Through Hole ◽  
Voltage Gradients ◽  
Ic Package ◽  
Through Hole ◽  
Failure Localization

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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