Drosophila embryo as experimental model: lessons learnt from genes in axis formation

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.

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Evidence for a highly selective RNA transport system and its role in establishing the dorsoventral axis of the Drosophila egg

Development ◽

10.1242/dev.114.3.653 ◽

1992 ◽

Vol 114 (3) ◽

pp. 653-661 ◽

Cited By ~ 14

Author(s):

H.K. Cheung ◽

T.L. Serano ◽

R.S. Cohen

Keyword(s):

Dorsal Surface ◽

Drosophila Embryo ◽

Follicle Cells ◽

Oocyte Nucleus ◽

Axis Formation ◽

Asymmetric Distribution ◽

Rna Transport ◽

Nurse Cells ◽

Dorsoventral Axis ◽

Multistep Process

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)

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Ultrastructural Alterations in Sinusoidal Endothelial Fenestrae as a Result of Hypoxia

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100090828 ◽

1976 ◽

Vol 34 ◽

pp. 168-169

Author(s):

Waykin Nopanitaya ◽

Raeford E. Brown ◽

Joe W. Grisham ◽

Johnny L. Carson

Keyword(s):

Endothelial Cells ◽

Experimental Model ◽

Hepatic Lobule ◽

Ultrastructural Alterations ◽

Large Type ◽

Sinusoidal Endothelial Fenestrae ◽

General Size ◽

Sem Studies

Mammalian endothelial cells lining hepatic sinusoids have been found to be widely fenestrated. Previous SEM studies (1,2) have noted two general size catagories of fenestrations; large fenestrae were distributed randomly while the small type occurred in groups. These investigations also reported that large fenestrae were more numerous and larger in the endothelial cells at the afferent ends of sinusoids or around the portal areas, whereas small fenestrae were more numerous around the centrilobular portion of the hepatic lobule. It has been further suggested that under some physiologic conditions small fenestrae could fuse and subsequently become the large type, but this is, as yet, unproven.We have used a reproducible experimental model of hypoxia to study the ultrastructural alterations in sinusoidal endothelial fenestrations in order to investigate the origin of occurrence of large fenestrae.

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Laser scanning confocal microscopic analysis of cytoskeletal and nuclear reorganization in live Drosophila embryos

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100146710 ◽

1993 ◽

Vol 51 ◽

pp. 174-175

Author(s):

William Theurkauf

Keyword(s):

Laser Scanning ◽

Microscopic Analysis ◽

Large Cell ◽

Early Embryo ◽

Drosophila Embryo ◽

Cortical Actin ◽

Nuclear Reorganization ◽

Cytoskeletal Elements ◽

Microtubule Structure ◽

Drosophila Embryos

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.

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

Biochemical Society Transactions ◽

10.1042/bst20200298 ◽

2020 ◽

Vol 48 (3) ◽

pp. 1243-1253 ◽

Cited By ~ 1

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.

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