scholarly journals Pipe-Dependent Ventral Processing of Easter by Snake Is the Defining Step in Drosophila Embryo DV Axis Formation

2010 ◽  
Vol 20 (12) ◽  
pp. 1133-1137 ◽  
Author(s):  
Yong Suk Cho ◽  
Leslie M. Stevens ◽  
David Stein
2003 ◽  
Vol 13 (23) ◽  
pp. 2097-2102 ◽  
Author(s):  
Petros Ligoxygakis ◽  
Siegfried Roth ◽  
Jean-Marc Reichhart

Development ◽  
2002 ◽  
Vol 129 (12) ◽  
pp. 2965-2975 ◽  
Author(s):  
Francesca Peri ◽  
Martin Technau ◽  
Siegfried Roth

The restriction of Pipe, a potential glycosaminoglycan-modifying enzyme, to ventral follicle cells of the egg chamber is essential for dorsoventral axis formation in the Drosophila embryo. pipe repression depends on the TGFα-like ligand Gurken, which activates the Drosophila EGF receptor in dorsal follicle cells. An analysis of Raf mutant clones shows that EGF signalling is required cell-autonomously in all dorsal follicle cells along the anteroposterior axis of the egg chamber to repress pipe. However, the autoactivation of EGF signalling important for dorsal follicle cell patterning has no influence on pipe expression. Clonal analysis shows that also the mirror-fringe cassette suggested to establish a secondary signalling centre in the follicular epithelium is not involved in pipe regulation. These findings support the view that the pipe domain is directly delimited by a long-range Gurken gradient. Pipe induces ventral cell fates in the embryo via activation of the Spätzle/Toll pathway. However, large dorsal patches of ectopic pipe expression induced by Raf clones rarely affect embryonic patterning if they are separated from the endogenous pipe domain. This indicates that potent inhibitory processes prevent pipe dependent Toll activation at the dorsal side of the egg.


Development ◽  
1992 ◽  
Vol 114 (3) ◽  
pp. 653-661 ◽  
Author(s):  
H.K. Cheung ◽  
T.L. Serano ◽  
R.S. Cohen

The specification of cell fates along the dorsoventral axis of the Drosophila embryo is dependent on the asymmetric distribution of proteins within the egg and within the egg's outer membranes. Such asymmetries arise during oogenesis and are dependent on multiple cell-cell interactions between the developing oocyte and its neighboring somatic follicle cells. The earliest known such interaction involves the generation of a signal in the oocyte and its reception in the follicle cells lying on the dorsal surface of the oocyte at approximately stage 10 of oogenesis. Several independent lines of investigation indicate that the fs(1)K10 (K10) gene negatively regulates the synthesis of the signal in the oocyte nucleus. Here we present data that indicate that the accumulation of K10 protein in the oocyte nucleus is a multistep process involving: (1) the synthesis of K10 RNA in nurse cells, (2) the rapid transport of K10 RNA from nurse cells into the oocyte, (3) the localization of K10 RNA to the anterior margin of the oocyte, and (4) K10 protein synthesis and localization. K10 RNA is transported into the oocyte continuously beginning at approximately stage 2. This indicates a high degree of selectivity in transport, since most RNAs synthesized in stage 2 and older nurse cells are stored there until stage 11, when nurse cells donate their entire cytoplasm to the oocyte. The sequences responsible for the early (pre-stage 11) and selective transport of K10 RNA into the oocyte map to the 3' transcribed non-translated region of the gene. None of the other identified genes involved in dorsoventral axis formation are required for K10 RNA transport.(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
William Theurkauf

Cell division in eucaryotes depends on coordinated changes in nuclear and cytoskeletal components. In Drosophila melanogaster embryos, the first 13 nuclear divisions occur without cytokinesis. During the final four divisions, nuclei divide in a uniform monolayer at the surface of the embryo. These surface divisions are accompanied by dramatic changes in cortical actin and microtubule structure (Karr and Alberts, 1986), and inhibitor studies indicate that these changes are essential to orderly mitosis (Zalokar and Erk, 1976). Because the early embryo is syncytial, fluorescent probes introduced by microinjection are incorporated in structures associated with all of the nuclei in the blastoderm. In addition, the nuclei divide synchronously every 10 to 20 min. These characteristics make the syncytial blastoderm embryo an excellent system for the analysis of mitotic reorganization of both nuclear and cytoskeletal elements. However, the Drosophila embryo is a large cell, and resolution of cytoskeletal filaments and nuclear structure is hampered by out-of focus signal.


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.


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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