scholarly journals Partial rescue of dorsal , a maternal effect mutation affecting the dorso-ventral pattern of the Drosophila embryo, by the injection of wild-type cytoplasm

1983 ◽  
Vol 2 (10) ◽  
pp. 1695-1699 ◽  
Author(s):  
Pedro Santamaria ◽  
Christiane Nüsslein-Volhard
Keyword(s):  
Maternal Effect ◽  
Drosophila Embryo ◽  
Wild Type

Activation of the easter zymogen is regulated by five other genes to define dorsal-ventral polarity in the Drosophila embryo

Development ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 607-616 ◽  
Author(s):  
R. Chasan ◽  
Y. Jin ◽  
K.V. Anderson
Keyword(s):  
Maternal Effect ◽  
Serine Proteases ◽  
Drosophila Embryo ◽  
Vitelline Membrane ◽  
Mutant Form ◽  
Wild Type ◽  
Zymogen Activation ◽  
Embryonic Polarity ◽  
Dominant Mutant ◽  
Maternal Effect Genes

The product of the Drosophila easter gene, a member of the trypsin family of serine proteases, must be more active ventrally than dorsally to promote normal embryonic polarity. The majority of the easter protein in the embryo is present in the unprocessed zymogen form and appears to be evenly distributed in the extracellular space, indicating that the asymmetric activity of wild-type easter must arise post-translationally. A dominant mutant form of easter that does not require cleavage of the zymogen for activity (ea delta N) is active both dorsally and ventrally. The ea delta N mutant bypasses the requirement for five other maternal effect genes, indicating that these five genes exert their effects on dorsal-ventral patterning solely by controlling the activation of the easter zymogen. We propose that dorsal-ventral asymmetry is initiated by a ventrally-localized molecule in the vitelline membrane that nucleates an easter zymogen activation complex, leading to the production of ventrally active easter enzyme.

Analysis of maternal effect mutant combinations elucidates regulation and function of the overlap of hunchback and Kruppel gene expression in the Drosophila blastoderm embryo

Development ◽  
1989 ◽  
Vol 107 (3) ◽  
pp. 651-662 ◽  
Author(s):  
U. Gaul ◽  
H. Jackle
Keyword(s):  
Maternal Effect ◽  
Drosophila Embryo ◽  
Homeotic Genes ◽  
Protein Distribution ◽  
Wild Type ◽  
Gap Gene ◽  
Gap Genes ◽  
Underlying Mechanisms ◽  
And Function ◽  
Pair Rule

The metameric organisation of the Drosophila embryo is generated early during development, due to the action of maternal effect and zygotic segmentation and homeotic genes. The gap genes participate in the complex process of pattern formation by providing a link between the maternal and the zygotic gene activities. Under the influence of maternal gene products they become expressed in distinct domains along the anteroposterior axis of the embryo; negative interactions between neighboring gap genes are thought to be involved in establishing the expression domains. The gap gene activities in turn are required for the correct patterning of the pair-rule genes; little is known, however, about the underlying mechanisms. We have monitored the distribution of gap and pair-rule genes in wild-type embryos and in embryos in which the anteroposterior body pattern is greatly simplified due to combinations of maternal effect mutations (staufen exuperantia, vasa exuperantia, vasa exuperantia, bicoid oskar, bicoid oskar torsolike, vasa torso exuperantia). We show that the domains of protein distribution of the gap genes hunchback and Kruppel overlap in wild-type embryos. Based on the analysis of the maternal mutant combinations, we suggest an explanation of how this overlap is generated. Furthermore, our data show that different constellations of gap gene activities provide different input for the pair-rule genes, and thus strongly suggest that the overlap of hunchback and Kruppel in wild-type is functional in the formation of the patterns of pair-rule genes.

A group of genes required for maintenance of the amnioserosa tissue in Drosophila

Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1343-1352 ◽  
Author(s):  
L.H. Frank ◽  
C. Rushlow
Keyword(s):  
Cell Death ◽  
Cell Loss ◽  
Dorsal Side ◽  
Drosophila Embryo ◽  
Epithelial Tissue ◽  
Dorsoventral Patterning ◽  
Wild Type ◽  
Germ Band ◽  
Initial Development

The amnioserosa is an extraembryonic, epithelial tissue that covers the dorsal side of the Drosophila embryo. The initial development of the amnioserosa is controlled by the dorsoventral patterning genes. Here we show that a group of genes, which we refer to as the U-shaped-group (ush-group), is required for maintenance of the amnioserosa tissue once it has differentiated. Using several molecular markers, we examined amnioserosa development in the ush-group mutants: u-shaped (ush), hindsight (hnt), serpent (srp) and tail-up (tup). Our results show that the amnioserosa in these mutants is specified correctly and begins to differentiate as in wild type. However, following germ-band extension, there is a premature loss of the amnioserosa. We demonstrate that this cell loss is a consequence of programmed cell death (apoptosis) in ush, hnt and srp, but not in tup. We discuss the role of the ush-group genes in maintaining the amnioserosa's viability. We also discuss a possible role for the amnioserosa in germ-band retraction in light of these mutants' unretracted phenotype.

Muscle development is independent of innervation during Drosophila embryogenesis

Development ◽  
1993 ◽  
Vol 119 (2) ◽  
pp. 533-543 ◽  
Author(s):  
K. Broadie ◽  
M. Bate
Keyword(s):  
Time Course ◽  
Muscle Development ◽  
Single Cells ◽  
Drosophila Embryo ◽  
Wild Type ◽  
Type Pattern ◽  
Motor Nerves ◽  
Embryonic Myogenesis ◽  
Peripheral Motor

We have examined the role of innervation in directing embryonic myogenesis, using a mutant (prospero), which delays the pioneering of peripheral motor nerves of the Drosophila embryo. In the absence of motor nerves, myoblasts fuse normally to form syncytial myotubes, myotubes form normal attachments to the epidermis, and a larval musculature comparable to the wild-type pattern is generated and maintained. Likewise, the twist-expressing myoblasts that prefigure the adult musculature segregate normally in the absence of motor nerves, migrate to their final embryonic positions and continue to express twist until the end of embryonic development. In the absence of motor nerves, myotubes uncouple at the correct developmental stage to form single cells. Subsequently, uninnervated myotubes develop the mature electrical and contractile properties of larval muscles with a time course indistinguishable from normally innervated myotubes. We conclude that innervation plays no role in the patterning, morphogenesis, maintenance or physiological development of the somatic muscles in the Drosophila embryo.

Homeostatic balance between dorsal and cactus proteins in the Drosophila embryo

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 135-148 ◽  
Author(s):  
S. Govind ◽  
L. Brennan ◽  
R. Steward
Keyword(s):  
Direct Interaction ◽  
Drosophila Embryo ◽  
Loss Of Function ◽  
Wild Type ◽  
Wild Type Embryo ◽  
Cleavage Stage ◽  
Dorsoventral Axis ◽  
Maternal Effect Gene ◽  
Early Embryos ◽  
Effect Gene

The maternal-effect gene dorsal encodes the ventral morphogen that is essential for elaboration of ventral and ventrolateral fates in the Drosophila embryo. Dorsal belongs to the rel family of transcription factors and controls asymmetric expression of zygotic genes along the dorsoventral axis. The dorsal protein is cytoplasmic in early embryos, possibly because of a direct interaction with cactus. In response to a ventral signal, dorsal protein becomes partitioned into nuclei of cleavage-stage syncytial blastoderms such that the ventral nuclei have the maximum amount of dorsal protein, and the lateral and dorsal nuclei have progressively less protein. Here we show that transgenic flies containing the dorsal cDNA, which is driven by the constitutively active hsp83 promoter, exhibits rescue of the dorsal- phenotype. Transformed lines were used to increase the level of dorsal protein. Females with dorsal levels roughly twice that of wild-type produced normal embryos, while a higher level of dorsal protein resulted in phenotypes similar to those observed for loss-of-function cactus mutations. By manipulating the cactus gene dose, we found that in contrast to a dorsal/cactus ratio of 2.5 which resulted in fully penetrant weak ventralization, a cactus/dorsal ratio of 3.0 was acceptable by the system. By manipulating dorsal levels in different cactus and dorsal group mutant backgrounds, we found that the relative amounts of ventral signal to that of the dorsal-cactus complex is important for the elaboration of the normal dorsoventral pattern. We propose that in a wild-type embryo, the activities of dorsal and cactus are not independently regulated; excess cactus activity is deployed only if a higher level of dorsal protein is available. Based on these results we discuss how the ventral signal interacts with the dorsal-cactus complex, thus forming a gradient of nuclear dorsal protein.

Biphasic activation of the BMP pathway patterns the Drosophila embryonic dorsal region

Development ◽  
2001 ◽  
Vol 128 (6) ◽  
pp. 965-972 ◽  
Author(s):  
R. Dorfman ◽  
B.Z. Shilo
Keyword(s):  
Inhibitory Activity ◽  
Early Phase ◽  
Drosophila Embryo ◽  
Activation Pattern ◽  
Wild Type ◽  
Germ Band ◽  
Dorsal Region ◽  
Bmp Pathway ◽  
Simultaneous Activation ◽  
Blastoderm Stage

The BMP pathway patterns the dorsal region of the Drosophila embryo. Using an antibody recognizing phosphorylated Mad (pMad), we followed signaling directly. In wild-type embryos, a biphasic activation pattern is observed. At the cellular blastoderm stage high pMad levels are detected only in the dorsal-most cell rows that give rise to amnioserosa. This accumulation of pMad requires the ligand Screw (Scw), the Short gastrulation (Sog) protein, and cleavage of their complex by Tolloid (Tld). When the inhibitory activity of Sog is removed, Mad phosphorylation is expanded. In spite of the uniform expression of Scw, pMad expansion is restricted to the dorsal domain of the embryo where Dpp is expressed. This demonstrates that Mad phosphorylation requires simultaneous activation by Scw and Dpp. Indeed, the early pMad pattern is abolished when either the Scw receptor Saxophone (Sax), the Dpp receptor Thickveins (Tkv), or Dpp are removed. After germ band extension, a uniform accumulation of pMad is observed in the entire dorsal domain of the embryo, with a sharp border at the junction with the neuroectoderm. From this stage onward, activation by Scw is no longer required, and Dpp suffices to induce high levels of pMad. In these subsequent phases pMad accumulates normally in the presence of ectopic Sog, in contrast to the early phase, indicating that Sog is only capable of blocking activation by Scw and not by Dpp.

Genes that control dorsoventral polarity affect gene expression along the anteroposterior axis of the Drosophila embryo

Development ◽  
1987 ◽  
Vol 99 (3) ◽  
pp. 327-332 ◽  
Author(s):  
S.B. Carroll ◽  
G.M. Winslow ◽  
V.J. Twombly ◽  
M.P. Scott
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Maternal Effect ◽  
Positional Information ◽  
Drosophila Embryo ◽  
Dorsoventral Polarity ◽  
Anteroposterior Axis ◽  
Positional Marker ◽  
Control Pattern ◽  
The Relationship

At least 13 genes control the establishment of dorsoventral polarity in the Drosophila embryo and more than 30 genes control the anteroposterior pattern of body segments. Each group of genes is thought to control pattern formation along one body axis, independently of the other group. We have used the expression of the fushi tarazu (ftz) segmentation gene as a positional marker to investigate the relationship between the dorsoventral and anteroposterior axes. The ftz gene is normally expressed in seven transverse stripes. Changes in the striped pattern in embryos mutant for other genes (or progeny of females homozygous for maternal-effect mutations) can reveal alterations of cell fate resulting from such mutations. We show that in the absence of any of ten maternal-effect dorsoventral polarity gene functions, the characteristic stripes of ftz protein are altered. Normally there is a difference between ftz stripe spacing on the dorsal and ventral sides of the embryo; in dorsalized mutant embryos the ftz stripes appear to be altered so that dorsal-type spacing occurs on all sides of the embryo. These results indicate that cells respond to dorsoventral positional information in establishing early patterns of gene expression along the anteroposterior axis and that there may be more significant interactions between the different axes of positional information than previously determined.

scholarly journals Ventralization of the Drosophila embryo by deletion of extracellular leucine-rich repeats in the Toll protein.

1995 ◽  
Vol 6 (5) ◽  
pp. 587-596 ◽  
Author(s):  
K A Winans ◽  
C Hashimoto
Keyword(s):  
Cell Fate ◽  
Transmembrane Protein ◽  
Signal Transduction Pathway ◽  
Extracellular Domain ◽  
Drosophila Embryo ◽  
Transduction Pathway ◽  
Wild Type ◽  
Truncated Form ◽  
Biochemical Analyses ◽  
Leucine Rich Repeats

Dorsoventral polarity of the Drosophila embryo is established by a signal transduction pathway in which the maternal transmembrane protein Toll appears to function as the receptor for a ventrally localized extracellular ligand. Certain dominant Toll alleles encode proteins that behave as partially ligand-independent receptors, causing embryos containing these proteins to become ventralized. In extracts of embryos derived from mothers carrying these dominant alleles, we detected a polypeptide of approximately 35 kDa in addition to full-length Toll polypeptides with antibodies to Toll. Our biochemical analyses suggest that the smaller polypeptide is a truncated form of Toll lacking extracellular domain sequences. To assay the biological activity of such a shortened form of Toll, we synthesized RNA encoding a mutant polypeptide lacking the leucine-rich repeats that comprise most of Toll's extracellular domain and injected this RNA into embryos. The truncated Toll protein elicited the most ventral cell fate independently of the wild-type Toll protein and its ligand. These results support the view that Toll is a receptor whose extracellular domain regulates the intrinsic signaling activity of its cytoplasmic domain.

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