Drosophila-Raf Acts to Elaborate Dorsoventral Pattern in the Ectoderm of Developing Embryos

Genetics ◽  
2001 ◽  
Vol 159 (3) ◽  
pp. 1031-1044
Author(s):  
Kori Radke ◽  
Kimberly Johnson ◽  
Rong Guo ◽  
Anne Davidson ◽  
Linda Ambrosio
Keyword(s):  
Egf Receptor ◽  
Drosophila Embryo ◽  
Functional Requirements ◽  
Loss Of Function ◽  
Maternal Role ◽  
Partial Loss ◽  
Cell Fates ◽  
Regulatory Domains ◽  
Early Drosophila Embryo ◽  
Lateral Cell

Abstract In the early Drosophila embryo the activity of the EGF-receptor (Egfr) is required to instruct cells to adopt a ventral neuroectodermal fate. Using a gain-of-function mutation we showed that D-raf acts to transmit this and other late-acting embryonic Egfr signals. A novel role for D-raf was also identified in lateral cell development using partial loss-of-function D-raf mutations. Thus, we provide evidence that zygotic D-raf acts to specify cell fates in two distinct pathways that generate dorsoventral pattern within the ectoderm. These functional requirements for D-raf activity occur subsequent to its maternal role in organizing the anterioposterior axis. The consequences of eliminating key D-raf regulatory domains and specific serine residues in the transmission of Egfr and lateral epidermal signals were also addressed here.

EGF receptor signaling induces pointed P1 transcription and inactivates Yan protein in the Drosophila embryonic ventral ectoderm

Development ◽  
1996 ◽  
Vol 122 (11) ◽  
pp. 3355-3362 ◽  
Author(s):  
L. Gabay ◽  
H. Scholz ◽  
M. Golembo ◽  
A. Klaes ◽  
B.Z. Shilo ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Target Genes ◽  
Egf Receptor ◽  
Protein A ◽  
Drosophila Embryo ◽  
Cell Fates ◽  
Secondary Target ◽  
Graded Activity ◽  
Definition Of

The induction of different cell fates along the dorsoventral axis of the Drosophila embryo requires a graded activity of the EGF receptor tyrosine kinase (DER). Here we have identified primary and secondary target genes of DER, which mediate the determination of discrete ventral cell fates. High levels of DER activation in the ventralmost cells trigger expression of the transcription factors encoded by ventral nervous system defective (vnd) and pointed P1 (pntPl). Concomitant with the induction of pntP1, high levels of DER activity lead to inactivation of the Yan protein, a transcriptional repressor of Pointed-target genes. These two antagonizing transcription factors subsequently control the expression of secondary target genes such as otd, argos and tartan. The simultaneous effects of the DER pathway on pntP1 induction and Yan inactivation may contribute to the definition of the border of the ventralmost cell fates.

maelstrom is required for an early step in the establishment of Drosophila oocyte polarity: posterior localization of grk mRNA

Development ◽  
1997 ◽  
Vol 124 (22) ◽  
pp. 4661-4671 ◽  
Author(s):  
N.J. Clegg ◽  
D.M. Frost ◽  
M.K. Larkin ◽  
L. Subrahmanyan ◽  
Z. Bryant ◽  
...  
Keyword(s):  
Nurse Cell ◽  
Egf Receptor ◽  
Mrna Localization ◽  
Follicle Cells ◽  
Rna Transport ◽  
Nurse Cells ◽  
Loss Of Function ◽  
Cell Fates ◽  
Early Step ◽  
Novel Protein

We describe a mutant, maelstrom, that disrupts a previously unobserved step in mRNA localization within the early oocyte, distinct from nurse-cell-to-oocyte RNA transport. Mutations in maelstrom disturb the localization of mRNAs for Gurken (a ligand for the Drosophila Egf receptor), Oskar and Bicoid at the posterior of the developing (stage 3–6) oocyte. maelstrom mutants display phenotypes detected in gurken loss-of-function mutants: posterior follicle cells with anterior cell fates, bicoid mRNA localization at both poles of the stage 8 oocyte and ventralization of the eggshell. These data are consistent with the suggestion that early posterior localization of gurken mRNA is essential for activation of the Egf receptor pathway in posterior follicle cells. Posterior localization of mRNA in stage 3–6 oocytes could therefore be one of the earliest known steps in the establishment of oocyte polarity. The maelstrom gene encodes a novel protein that has a punctate distribution in the cytoplasm of the nurse cells and the oocyte until the protein disappears in stage 7 of oogenesis.

Cytological characterisation of the mutant phenotypes produced during early embryogenesis by null and loss-of-function alleles of the gammaTub37C gene in Drosophila

1999 ◽  
Vol 112 (5) ◽  
pp. 659-667 ◽  
Author(s):  
S. Llamazares ◽  
G. Tavosanis ◽  
C. Gonzalez
Keyword(s):  
Polar Body ◽  
Nuclear Proliferation ◽  
Early Embryogenesis ◽  
Drosophila Embryo ◽  
Loss Of Function ◽  
Female Meiosis ◽  
Polar Bodies ◽  
Early Drosophila Embryo ◽  
Gamma Tubulin ◽  
Mutant Phenotypes

We have studied the mutant phenotypes brought about during early embryogenesis by mutation in the gammaTub37C gene, one of the two isoforms of gamma-tubulin that have been identified in Drosophila. We have focused our attention on fs(2)TW1(1) and fs(2)TW1(RU34), a null and a hypomorph allele of this gene, whose sequences we report in this work. We have found that the abnormal meiotic figures observed in mutant stage 14 oocytes are not observed in laid oocytes or fertilised embryos, suggesting that these abnormal meiotic figures are not terminally arrested. We have also concluded that both null and hypomorph alleles lead to a total arrest of nuclear proliferation during early embryogenesis. This is in contrast to their effect on female meiosis-I where hypomorph alleles display a much weaker phenotype. Finally, we have observed that null and hypomorph alleles lead to some distinct phenotypes. Unfertilised laid oocytes and fertilised embryos deficient for gammaTub37C do not contain polar bodies and have a few bipolar microtubule arrays. In contrast, oocytes and embryos from weaker alleles do not have these microtubule arrays, but do contain polar bodies, or polar-body-like structures. These results indicate that gammaTub37C is essential for nuclear proliferation in the early Drosophila embryo.

The role of the NK-homeobox gene slouch (S59) in somatic muscle patterning

Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4525-4535 ◽  
Author(s):  
S. Knirr ◽  
N. Azpiazu ◽  
M. Frasch
Keyword(s):  
Muscle Development ◽  
Ectopic Expression ◽  
Homeobox Gene ◽  
Drosophila Embryo ◽  
Loss Of Function ◽  
Cell Fates ◽  
Somatic Muscle ◽  
Gene Encoding ◽  
Body Wall Muscles ◽  
Founder Cells

In the Drosophila embryo, a distinct class of myoblasts, designated as muscle founders, prefigures the mature pattern of somatic body wall muscles. Each founder cell appears to be instrumental in generating a single larval muscle with a defined identity. The NK homeobox gene S59 was the first of a growing number of proposed ‘identity genes’ that have been found to be expressed in stereotyped patterns in specific subsets of muscle founders and their progenitor cells and are thought to control their developmental fates. In the present study, we describe the effects of gain- and loss-of-function experiments with S59. We find that a null mutation in the gene encoding S59, which we have named slouch (slou), disrupts the development of all muscles that are derived from S59-expressing founder cells. The observed phenotypes upon mutation and ectopic expression of slouch include transformations of founder cell fates, thus confirming that slouch (S59) functions as an identity gene in muscle development. These fate transformations occur between sibling founder cells as well as between neighboring founders that are not lineage-related. In the latter case, we show that slouch (S59) activity is required cell-autonomously to repress the expression of ladybird (lb) homeobox genes, thereby preventing specification along the lb pathway. Together, these findings provide new insights into the regulatory interactions that establish the somatic muscle pattern.

scholarly journals Decoding temporal interpretation of the morphogen Bicoid in the early Drosophila embryo

2017 ◽  
Author(s):  
Anqi Huang ◽  
Christopher Amourda ◽  
Shaobo Zhang ◽  
Nicholas S. Tolwinski ◽  
Timothy E. Saunders
Keyword(s):  
Cell Fate ◽  
Spatial Information ◽  
Drosophila Embryo ◽  
High Temporal Resolution ◽  
Local Concentration ◽  
Cell Fates ◽  
Cell Fate Decisions ◽  
Gap Gene ◽  
Early Drosophila Embryo ◽  
Time Specific

SUMMARYMorphogen gradients provide essential spatial information during development. Not only the local concentration but also duration of morphogen exposure is critical for correct cell fate decisions. Yet, how and when cells temporally integrate signals from a morphogen remains unclear. Here, we use optogenetic manipulation to switch off Bicoid-dependent transcription in the early Drosophila embryo with high temporal resolution, allowing time-specific and reversible manipulation of morphogen signalling. We find that Bicoid transcriptional activity is dispensable for embryonic viability in the first hour after fertilization, but persistently required throughout the rest of the blastoderm stage. Short interruptions of Bicoid activity alter the most anterior cell fate decisions, while prolonged inactivation expands patterning defects from anterior to posterior. Such anterior susceptibility correlates with high reliance of anterior gap gene expression on Bicoid. Therefore, cell fates exposed to higher Bicoid concentration require input for longer duration, demonstrating a previously unknown aspect of morphogen decoding.

scholarly journals Decoding temporal interpretation of the morphogen Bicoid in the early Drosophila embryo

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Anqi Huang ◽  
Christopher Amourda ◽  
Shaobo Zhang ◽  
Nicholas S Tolwinski ◽  
Timothy E Saunders
Keyword(s):  
Cell Fate ◽  
Spatial Information ◽  
Drosophila Embryo ◽  
High Temporal Resolution ◽  
Local Concentration ◽  
Cell Fates ◽  
Cell Fate Decisions ◽  
Gap Gene ◽  
Early Drosophila Embryo ◽  
Time Specific

Morphogen gradients provide essential spatial information during development. Not only the local concentration but also duration of morphogen exposure is critical for correct cell fate decisions. Yet, how and when cells temporally integrate signals from a morphogen remains unclear. Here, we use optogenetic manipulation to switch off Bicoid-dependent transcription in the early Drosophila embryo with high temporal resolution, allowing time-specific and reversible manipulation of morphogen signalling. We find that Bicoid transcriptional activity is dispensable for embryonic viability in the first hour after fertilization, but persistently required throughout the rest of the blastoderm stage. Short interruptions of Bicoid activity alter the most anterior cell fate decisions, while prolonged inactivation expands patterning defects from anterior to posterior. Such anterior susceptibility correlates with high reliance of anterior gap gene expression on Bicoid. Therefore, cell fates exposed to higher Bicoid concentration require input for longer duration, demonstrating a previously unknown aspect of Bicoid decoding.

scholarly journals Hairless is a cofactor for Runt-dependent transcriptional regulation

2011 ◽  
Vol 22 (8) ◽  
pp. 1364-1374 ◽  
Author(s):  
Pegine B. Walrad ◽  
Saiyu Hang ◽  
J. Peter Gergen
Keyword(s):  
Transcriptional Regulation ◽  
Molecular Interactions ◽  
Target Gene ◽  
Transcriptional Regulator ◽  
Drosophila Embryo ◽  
Functional Requirements ◽  
Developmental Pathway ◽  
Downstream Target ◽  
Early Drosophila Embryo ◽  
Cellular Context

Runt is a vital transcriptional regulator in the developmental pathway responsible for segmentation in the Drosophila embryo. Runt activates or represses transcription in a manner that is dependent on both cellular context and the specific downstream target. Here we identify Hairless (H) as a Runt-interacting molecule that functions during segmentation. We find that H is important for maintenance of engrailed (en) repression as was previously demonstrated for Groucho (Gro), Rpd3, and CtBP. H also contributes to the Runt-dependent repression of sloppy-paired-1 (slp1), a role that is not shared with these other corepressors. We further find distinct roles for these different corepressors in the regulation of other Runt targets in the early Drosophila embryo. These findings, coupled with observations on the distinct functional requirements for Runt in regulating these several different targets, indicate that Runt-dependent regulation in the Drosophila blastoderm embryo relies on unique, target-gene-specific molecular interactions.

scholarly journals The Tailless Nuclear Receptor Acts as a Dedicated Repressor in the Early Drosophila Embryo

2006 ◽  
Vol 26 (9) ◽  
pp. 3446-3454 ◽  
Author(s):  
Érica Morán ◽  
Gerardo Jiménez
Keyword(s):  
Nuclear Receptors ◽  
Nuclear Receptor ◽  
Target Genes ◽  
Activation Function ◽  
Drosophila Embryo ◽  
Intact Protein ◽  
Positive Interactions ◽  
Orphan Nuclear Receptor ◽  
Loss Of Function ◽  
Early Drosophila Embryo

ABSTRACT Tailless is an orphan nuclear receptor that controls terminal body patterning in Drosophila. Genetic analyses have revealed both positive and negative regulatory interactions of Tailless with various target genes, leading to the idea that, like many other nuclear receptors, Tailless mediates both activation and repression of transcription. In this paper, we have examined the consequences of converting Tailless into an obligate repressor and compared the activities of the resulting protein with those of wild-type Tailless. We find that this repressor form of Tailless behaves like the intact protein in gain- and loss-of-function experiments, being sufficient to support normal embryonic development and establish accurate patterns of gene expression even for positive Tailless targets such as hunchback and brachyenteron. This suggests that Tailless functions exclusively as a transcriptional repressor in the embryo and that the observed positive interactions of Tailless with specific targets are secondary effects involving repression of repressors. We provide evidence that knirps is one such repressor gene acting between Tailless and its indirect positive targets. Finally, our results indicate that Tailless exerts an active mechanism of repression via its ligand-binding domain and that this activity is largely independent of the activation function 2 (AF2) motif characteristic of most nuclear receptors.

Mechanisms of Gurken-dependentpiperegulation and the robustness of dorsoventral patterning inDrosophila

Development ◽  
2002 ◽  
Vol 129 (12) ◽  
pp. 2965-2975 ◽  
Author(s):  
Francesca Peri ◽  
Martin Technau ◽  
Siegfried Roth
Keyword(s):  
Egf Receptor ◽  
Follicle Cell ◽  
Dorsal Side ◽  
Drosophila Embryo ◽  
Follicle Cells ◽  
Follicular Epithelium ◽  
Axis Formation ◽  
Embryonic Patterning ◽  
Cell Fates ◽  
Egg Chamber

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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