Pattern formation under the control of the terminal system in the Drosophila embryo

Development ◽  
1990 ◽  
Vol 110 (2) ◽  
pp. 621-628 ◽  
Author(s):  
J. Casanova
Keyword(s):  
Pattern Formation ◽  
Tyrosine Kinase ◽  
Protein A ◽  
Primary Response ◽  
The Body ◽  
Drosophila Embryo ◽  
Tyrosine Kinase Receptor ◽  
Terminal System ◽  
Gap Genes

The specification of the most anterior and posterior domains of the Drosophila embryo depends on the activity of the torso protein, a putative tyrosine kinase receptor. Localized torso activity at the poles of the embryo generates graded information that specifies distinct portions of the body. The primary response to the terminal signal in the posterior end of the embryo is likely to be the activation of the gap genes huckebein and tailless. Here I address the question of how the graded maternal signal generates different elements of the pattern at the posterior end of the embryo and what role huckebein and tailless activities may play in this process. These experiments show that distinctly localized activities of huckebein and tailless are responsible for the appropriate expression of other genes known to be under the control of the terminal system. Moreover, they suggest that different elements of the terminal pattern can be specified in response to distinct levels of graded tailless activity.

scholarly journals Activation of an enhancer on the syndecan-1 gene is restricted to fibroblast growth factor family members in mesenchymal cells.

1997 ◽  
Vol 17 (6) ◽  
pp. 3210-3219 ◽  
Author(s):  
P Jaakkola ◽  
T Vihinen ◽  
A Määttä ◽  
M Jalkanen
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Mutational Analysis ◽  
Biological Effects ◽  
Protein A ◽  
Cell Types ◽  
Regulatory Elements ◽  
Tyrosine Kinase Receptor ◽  
Fibroblast Growth

Fibroblast growth factors (FGFs) induce a variety of biological effects on different cell types. They activate a number of genes, including immediate-early genes, such as the transcription factors Fos and Jun, which are also common targets for other tyrosine kinase receptor-activating growth factors. Here we describe a secondary far-upstream enhancer on the syndecan-1 gene that is activated only by members of the FGF family in NIH 3T3 cells, not by other receptor tyrosine kinase-activating growth factors (e.g., epidermal growth factor, platelet-derived growth factor, insulin-like growth factor, or serum). This FGF-inducible response element (FiRE) consists of a 170-bp array of five DNA motifs which bind two FGF-inducible Fos-Jun heterodimers, one inducible AP-2-related protein, a constitutively expressed upstream stimulatory factor, and one constitutive 46-kDa transcription factor. Mutational analysis showed that both AP-1 binding motifs are required, but not sufficient, for FiRE activation. Moreover, agents such as 12-O-tetradecanoylphorbol-13-acetate, okadaic acid, or forskolin, which are known to activate AP-1 complexes and AP-1-driven promoters, fail to activate FiRE. However, FiRE can be activated by the tyrosine kinase phosphatase inhibitor orthovanadate. Taken together, this data implies a differential activation of growth factor-initiated signaling on AP-1-driven regulatory elements.

scholarly journals Dynamic Maternal Gradients Control Timing and Shift-Rates forDrosophilaGap Gene Expression

2016 ◽  
Author(s):  
Berta Verd ◽  
Anton Crombach ◽  
Johannes Jaeger
Keyword(s):  
Gene Expression ◽  
Gene Regulation ◽  
Drosophila Melanogaster ◽  
Pattern Formation ◽  
Dynamic Process ◽  
Gene Expression Pattern ◽  
The Body ◽  
Transient Dynamics ◽  
Gap Gene ◽  
Gap Genes

AbstractPattern formation during development is a highly dynamic process. In spite of this, few experimental and modelling approaches take into account the explicit time-dependence of the rules governing regulatory systems. We address this problem by studying dynamic morphogen interpretation by the gap gene network inDrosophila melanogaster. Gap genes are involved in segment determination during early embryogenesis. They are activated by maternal morphogen gradients encoded bybicoid (bcd)andcaudal (cad). These gradients decay at the same time-scale as the establishment of the antero-posterior gap gene pattern. We use a reverse-engineering approach, based on data-driven regulatory models called gene circuits, to isolate and characterise the explicitly time-dependent effects of changing morphogen concentrations on gap gene regulation. To achieve this, we simulate the system in the presence and absence of dynamic gradient decay. Comparison between these simulations reveals that maternal morphogen decay controls the timing and limits the rate of gap gene expression. In the anterior of the embyro, it affects peak expression and leads to the establishment of smooth spatial boundaries between gap domains. In the posterior of the embryo, it causes a progressive slow-down in the rate of gap domain shifts, which is necessary to correctly position domain boundaries and to stabilise the spatial gap gene expression pattern. We use a newly developed method for the analysis of transient dynamics in non-autonomous (time-variable) systems to understand the regulatory causes of these effects. By providing a rigorous mechanistic explanation for the role of maternal gradient decay in gap gene regulation, our study demonstrates that such analyses are feasible and reveal important aspects of dynamic gene regulation which would have been missed by a traditional steady-state approach. More generally, it highlights the importance of transient dynamics for understanding complex regulatory processes in development.Author SummaryAnimal development is a highly dynamic process. Biochemical or environmental signals can cause the rules that shape it to change over time. We know little about the effects of such changes. For the sake of simplicity, we usually leave them out of our models and experimental assays. Here, we do exactly the opposite. We characterise precisely those aspects of pattern formation caused by changing signalling inputs to a gene regulatory network, the gap gene system ofDrosophila melanogaster. Gap genes are involved in determining the body segments of flies and other insects during early development. Gradients of maternal morphogens activate the expression of the gap genes. These gradients are highly dynamic themselves, as they decay while being read out. We show that this decay controls the peak concentration of gap gene products, produces smooth boundaries of gene expression, and slows down the observed positional shifts of gap domains in the posterior of the embryo, thereby stabilising the spatial pattern. Our analysis demonstrates that the dynamics of gene regulation not only affect the timing, but also the positioning of gene expression. This suggests that we must pay closer attention to transient dynamic aspects of development than is currently the case.

The torso pathway in Drosophila: a model system to study receptor tyrosine kinase signal transduction

Development ◽  
1993 ◽  
Vol 119 (Supplement) ◽  
pp. 47-56 ◽  
Author(s):  
Xiangyi Lu ◽  
Lizabeth A. Perkins ◽  
Norbert Perrimon
Keyword(s):  
Signal Transduction ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Current Knowledge ◽  
Current Model ◽  
Drosophila Embryo ◽  
Receptor Protein ◽  
Future Research ◽  
Threonine Kinase ◽  
Gap Genes

In the Drosophila embryo, specification of terminal cell fates that result in the formation of both the head (acron) and tail (telson) regions is under the control of the torso (tor) receptor tyrosine kinase. The current knowledge suggests that activation of tor at the egg pole initiates a signal transduction pathway that is mediated sequentially by the guanine nucleotide releasing factor son of sevenless (Sos), the p21Ras1 GTPase, the serine/threonine kinase D-raf and the tyrosine/threonine kinase MAPKK (Dsor1). Subsequently, it is postulated that activation, possibly by phosphorylation, of a transcription factor at the egg poles activates the transcription of the terminal gap genes tailless and huckebein. These gap genes, which encode putative transcription factors, then control the expression of more downstream factors that ultimately result in head and tail differentiation. Also involved in tor signaling is the non-receptor protein tyrosine phosphatase corkscrew (csw). Here, we review the current model and discuss future research directions in this field.

Torso signalling regulates terminal patterning in Drosophila by antagonising Groucho-mediated repression

Development ◽  
1997 ◽  
Vol 124 (19) ◽  
pp. 3827-3834 ◽  
Author(s):  
Z. Paroush ◽  
S.M. Wainwright ◽  
D. Ish-Horowicz
Keyword(s):  
Gene Expression ◽  
Dna Binding ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Drosophila Embryo ◽  
Gap Gene ◽  
Gap Genes ◽  
Developmental Contexts

Patterning of the non-segmental termini of the Drosophila embryo depends on signalling via the Torso receptor tyrosine kinase (RTK). Activation of Torso at the poles of the embryo triggers restricted expression of the zygotic gap genes tailless (tll) and huckebein (hkb). In this paper, we show that the Groucho (Gro) corepressor acts in this process to confine terminal gap gene expression to the embryonic termini. Embryos lacking maternal gro activity display ectopic tll and hkb transcription; the former leads, in turn, to lack of abdominal expression of the Kruppel and knirps gap genes. We show that torso signalling permits terminal gap gene expression by antagonising Gro-mediated repression. Thus, the corepressor Gro is employed in diverse developmental contexts and, probably, by a variety of DNA-binding repressors.

scholarly journals Holes in the Plasma Membrane Mimic Torso-Like Perforin in Torso Tyrosine Kinase Receptor Activation in the Drosophila Embryo

Genetics ◽  
2018 ◽  
Vol 210 (1) ◽  
pp. 257-262 ◽  
Author(s):  
Alessandro Mineo ◽  
Esther Fuentes ◽  
Marc Furriols ◽  
Jordi Casanova
Keyword(s):  
Plasma Membrane ◽  
Tyrosine Kinase ◽  
Receptor Activation ◽  
Drosophila Embryo ◽  
Tyrosine Kinase Receptor

Breast Cancer Resistance Protein: A Potential Therapeutic Target for Cancer

2020 ◽  
Vol 21 ◽  
Author(s):  
Sonali Mehendale-Munj
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Resistance Protein ◽  
Protein A ◽  
The Body ◽  
Cancer Therapies ◽  
Cancer Resistance ◽  
Lung Cancers ◽  
Resistance Protein ◽  
Atp Regulation ◽  
Treatment Procedures

: Breast Cancer Resistance Protein (BCRP) is an efflux transporter responsible for causing multidrug re-sistance(MDR). It is known to expel many potent antineoplastic drugs, owing to its efflux function. Efflux of chemothera-peutics because of BCRP develops resistance to manydrugs, leading to failure in cancer treatment. BCRP plays an important role in physiology by protecting the organism from xenobiotics and other toxins. It is a half-transporter affiliated to theATP-binding cassette (ABC) superfamily of transporters, encoded by the gene ABCG2 and functions in response to adenosine triphosphate (ATP). Regulation of BCRP expression is critically controlled at molecular levels which help in maintaining the balance of xenobiotics and nutrients inside the body. Expression of BCRP can be found in brain, liver, lung cancers and acute myeloid leukemia (AML). Moreover, it is also expressed at high levels in stem cells and many cell lines. This frequent expression of BCRP has an impact on the treatment procedures and if not scrutinized may lead to failure of many cancer therapies.

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