scholarly journals Jeb/Alk signalling regulates the Lame duck GLI family transcription factor in the Drosophila visceral mesoderm

Development ◽  
2013 ◽  
Vol 140 (15) ◽  
pp. 3156-3166 ◽  
Author(s):  
D. Popichenko ◽  
F. Hugosson ◽  
C. Sjogren ◽  
M. Dogru ◽  
Y. Yamazaki ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Visceral Mesoderm ◽  
Lame Duck

scholarly journals Distinct Posttranscriptional Mechanisms Regulate the Activity of the Zn Finger Transcription Factor Lame duck during Drosophila Myogenesis

2006 ◽  
Vol 26 (4) ◽  
pp. 1414-1423 ◽  
Author(s):  
Hong Duan ◽  
Hanh T. Nguyen
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factor ◽  
Posttranslational Modifications ◽  
Target Genes ◽  
Nuclear Translocation ◽  
Protein Activity ◽  
Downstream Target ◽  
Muscle Formation ◽  
Lame Duck ◽  
Fusion Competent Myoblasts

ABSTRACT Skeletal muscle formation in Drosophila melanogaster requires two types of myoblasts, muscle founders and fusion-competent myoblasts. Lame duck (Lmd), a member of the Gli superfamily of transcription factors, is essential for the specification and differentiation of fusion-competent myoblasts. We report herein that appropriate levels of active Lmd protein are attained by a combination of posttranscriptional mechanisms. We provide evidence that two different regions of the Lmd protein are critical for modulating the balance between its nuclear translocation and its retention within the cytoplasm. Activation of the Lmd protein is also tempered by posttranslational modifications of the protein that do not detectably change its subcellular localization. We further show that overexpression of Lmd protein derivatives that are constitutively nuclear or hyperactive results in severe muscle defects. These findings underscore the importance of regulated Lmd protein activity in maintaining proper activation of downstream target genes, such as Mef2, within fusion-competent myoblasts.

scholarly journals Integrative analysis of the zinc finger transcription factor Lame duck in the Drosophila myogenic gene regulatory network

2012 ◽  
Vol 109 (50) ◽  
pp. 20768-20773 ◽  
Author(s):  
B. W. Busser ◽  
D. Huang ◽  
K. R. Rogacki ◽  
E. A. Lane ◽  
L. Shokri ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Gene Regulatory Network ◽  
Zinc Finger ◽  
Regulatory Network ◽  
Integrative Analysis ◽  
Zinc Finger Transcription Factor ◽  
Lame Duck ◽  
Gene Regulatory

scholarly journals Distinct roles and requirements for Ras pathway signaling in visceral versus somatic muscle founder specification

2018 ◽  
Author(s):  
Yiyun Zhou ◽  
Sarah E. Popadowski ◽  
Emily Deustchman ◽  
Marc S. Halfon
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
Somatic Muscle ◽  
Cell Specification ◽  
Ets Transcription Factors ◽  
Ras Pathway ◽  
Signaling Specificity ◽  
Visceral Mesoderm ◽  
Ras Effectors

ABSTRACTPleiotropic signaling pathways must somehow engender specific cellular responses. In the Drosophila mesoderm, Ras pathway signaling specifies muscle founder cells from among the broader population of myoblasts. For somatic muscles, this is an inductive process mediated by the ETS-domain downstream Ras effectors Pointed and Aop (Yan). We demonstrate here that for the circular visceral muscles, despite superficial similarities, a significantly different specification mechanism is at work. Not only is visceral founder cell specification not dependent on Pointed or Aop, but Ras pathway signaling in its entirety can be bypassed. Our results show that de-repression, not activation, is the predominant role of Ras signaling in the visceral mesoderm and that accordingly, Ras signaling is not required in the absence of repression. The key repressor acts downstream of the transcription factor Lameduck and is likely a member of the ETS transcription factor family. Our findings fit with a growing body of data that point to a complex interplay between the Ras pathway, ETS transcription factors, and enhancer binding as a critical mechanism for determining unique responses to Ras signaling.SUMMARYA fundamentally different mechanism is shown for how Ras signaling governs cell fate specification in the Drosophila somatic versus visceral mesoderms, providing insight into how signaling specificity is achieved.

scholarly journals Hand is a direct target of the forkhead transcription factor Biniou during Drosophila visceral mesoderm differentiation

2007 ◽  
Vol 7 (1) ◽  
pp. 49 ◽  
Author(s):  
Dmitry Popichenko ◽  
Julia Sellin ◽  
Marek Bartkuhn ◽  
Achim Paululat
Keyword(s):  
Transcription Factor ◽  
Forkhead Transcription Factor ◽  
Visceral Mesoderm ◽  
Direct Target

scholarly journals DamID transcriptional profiling identifies the Snail/Scratch transcription factor Kahuli as an Alk target in the Drosophila visceral mesoderm

Development ◽  
2021 ◽  
Vol 148 (23) ◽  
Author(s):  
Patricia Mendoza-Garcia ◽  
Swaraj Basu ◽  
Sanjay Kumar Sukumar ◽  
Badrul Arefin ◽  
Georg Wolfstetter ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Target Genes ◽  
Transcriptional Profiling ◽  
Rtk Signaling ◽  
Visceral Mesoderm ◽  
Anaplastic Lymphoma ◽  
Mrna And Protein Expression ◽  
Target Molecules ◽  
Target Binding

ABSTRACT Development of the Drosophila visceral muscle depends on Anaplastic Lymphoma Kinase (Alk) receptor tyrosine kinase (RTK) signaling, which specifies founder cells (FCs) in the circular visceral mesoderm (VM). Although Alk activation by its ligand Jelly Belly (Jeb) is well characterized, few target molecules have been identified. Here, we used targeted DamID (TaDa) to identify Alk targets in embryos overexpressing Jeb versus embryos with abrogated Alk activity, revealing differentially expressed genes, including the Snail/Scratch family transcription factor Kahuli (Kah). We confirmed Kah mRNA and protein expression in the VM, and identified midgut constriction defects in Kah mutants similar to those of pointed (pnt). ChIP and RNA-Seq data analysis defined a Kah target-binding site similar to that of Snail, and identified a set of common target genes putatively regulated by Kah and Pnt during midgut constriction. Taken together, we report a rich dataset of Alk-responsive loci in the embryonic VM and functionally characterize the role of Kah in the regulation of embryonic midgut morphogenesis.

serpent, a GATA-like transcription factor gene, induces fat-cell development in Drosophila melanogaster

Development ◽  
2001 ◽  
Vol 128 (7) ◽  
pp. 1193-1200
Author(s):  
S.A. Hayes ◽  
J.M. Miller ◽  
D.K. Hoshizaki
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
Body Wall ◽  
Body Wall Muscle ◽  
Ectopic Fat ◽  
Fat Cells ◽  
Transcription Factor Gene ◽  
Fat Cell ◽  
Factor Gene ◽  
Visceral Mesoderm

The GATA-like transcription factor gene serpent is necessary for embryonic fat-cell differentiation in Drosophila (Sam, S., Leise, W. and Hoshizaki, D. K. (1996) Mech. Dev. 60, 197–205) and has been proposed to function in a cell-fate choice between fat cell and somatic gonadal precursors (Moore, L. A., Broihier, H. T., Van Doren, M. and Lehmann, R. (1998) Development 125, 837–44; Riechmann, V., Irion, U., Wilson, R., Grosskortenhaus, R. and Leptin, M. (1997) Development 124, 2915–22). Here, we report that deregulated expression of serpent in the mesoderm induces the formation of ectopic fat cells and prevents the migration and coalescence of the somatic gonadal precursors. The ectopic fat cells do not arise from hyperproliferation of the primary fat-cell clusters but they do associate with the endogenous fat cells to form a fat body that is expanded in both the dorsal/ventral and anterior/posterior axes. Misexpression of serpent also affects the differentiation of muscle cells. Few body-wall muscle precursors are specified and there is a loss of most body-wall muscle fibers. The precursors of the visceral mesoderm are also absent and concomitantly the visceral muscle is absent. We suggest that the ectopic fat cells might originate from cells that have the potential, but do not normally, differentiate into fat cells or from cells that have acquired a fat-cell fate. In light of our results, we discuss the role of serpent in fat-cell specification and in cell fate choices.

scholarly journals DamID transcriptional profiling identifies the Snail/Scratch transcription factor Kahuli as Alk target in the Drosophila visceral mesoderm

2021 ◽  
Author(s):  
Patricia Mendoza-Garcia ◽  
Swaraj Basu ◽  
Sanjay Kumar Sukumar ◽  
Badrul Arefin ◽  
Georg Wolfstetter ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase Ii ◽  
Target Genes ◽  
Transcriptional Profiling ◽  
Functional Characterization ◽  
Visceral Mesoderm ◽  
Anaplastic Lymphoma ◽  
Target Molecules ◽  
Target Binding

AbstractDevelopment of the midgut visceral muscle of Drosophila crucially depends on Anaplastic Lymphoma Kinase (Alk) receptor tyrosine kinase (RTK) signalling, which is needed to specify founder cells (FCs) in the circular visceral mesoderm (VM). While activation of the Alk receptor by its ligand Jelly Belly (Jeb) is well characterized, only a small number of target molecules have been identified. Here, we assayed RNA polymerase II (Pol II) occupancy in VM cells by using the targeted DamID (TaDa) approach. To identify Alk targets we employed comparative analysis of embryos overexpressing Jeb versus embryos with abrogated Alk activity, revealing differential expression of a number of genes, including the Snail/Scratch family transcription factor Kahuli (Kah). Upon further in vivo validation, we confirmed that Alk signalling regulates Kah mRNA expression in the VM. We show that Kah mutants display defects in the formation of midgut constrictions, similar to that of pointed (pnt) mutants. Analysis of publicly available ChIP data defined a Kah target-binding site similar to that of Snail. In addition, we compared genes that were differentially expressed in Kah mutants with publicly available Kah- and Pnt-ChIP datasets identifying a set of common target genes putatively regulated by Kah and Pnt in midgut constriction. Taken together, we (i) report a rich dataset of Alk responsive loci in the embryonic VM, (ii) provide the first functional characterization of the Kah transcription factor, identifying a role in embryonic midgut constriction, and (iii) suggest a model in which Kah and Pnt cooperate in embryonic midgut morphogenesis.

A Drosophila protein related to the human zinc finger transcription factor PRDII/MBPI/HIV-EP1 is required for dpp signaling

Development ◽  
1995 ◽  
Vol 121 (10) ◽  
pp. 3393-3403 ◽  
Author(s):  
K. Staehling-Hampton ◽  
A.S. Laughon ◽  
F.M. Hoffmann
Keyword(s):  
Signal Transduction ◽  
Transcription Factor ◽  
Cell Fate ◽  
Related Factor ◽  
Homeodomain Protein ◽  
Tgf Beta ◽  
Wing Vein ◽  
Mesoderm Cell ◽  
Visceral Mesoderm ◽  
Vein Formation

Little is known about the signal transduction pathways by which cells respond to mammalian TGF-beta s or to decapentaplegic (dpp), a Drosophila TGF-beta-related factor. Here we describe the genetic and molecular characterization of Drosophila schnurri (shn), a putative transcription factor implicated in dpp signaling. The shn protein has eight zinc fingers and is related to a human transcription factor, PRDII/MBPI/HIV-EP1, that binds to nuclear factor-kappa B-binding sites and activates transcription from the HIV long terminal repeat (LTR). shn mRNA is expressed in a dynamic pattern in the embryo that includes most of the known target tissues of dpp, including the dorsal blastoderm, the mesodermal germlayer and parasegments 4 and 7 of the midgut. Mutations in shn affect several developmental processes regulated by dpp including induction of visceral mesoderm cell fate, dorsal/ventral patterning of the lateral ectoderm and wing vein formation. Absence of shn function blocks the expanded expression of the homeodomain protein bagpipe in the embryonic mesoderm caused by ectopic dpp expression, illustrating a requirement for shn function downstream of dpp action. We conclude that shn function is critical for cells to respond properly to dpp and propose that shn protein is the first identified downstream component of the signal transduction pathway used by dpp and its receptors.

Author response for "Identification of Retinal Ganglion Cell Types and Brain Nuclei expressing the transcription factor Brn3c/Pou4f3 using a Cre recombinase knock‐in allele"

2020 ◽  
Author(s):  
Nadia Parmhans ◽  
Anne Drury Fuller ◽  
Eileen Nguyen ◽  
Katherine Chuang ◽  
David Swygart ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Types ◽  
Cre Recombinase ◽  
Author Response ◽  
Retinal Ganglion ◽  
Brain Nuclei

Transcription factor/DNA interactions visualized by electron spectroscopic imaging

1992 ◽  
Vol 50 (1) ◽  
pp. 450-451
Author(s):  
David P. Bazett-Jones ◽  
Mark L. Brown
Keyword(s):  
Transcription Factor ◽  
Dna Sequences ◽  
Transcription Initiation ◽  
Molecular Mechanisms ◽  
Phosphorus Content ◽  
Spectroscopic Imaging ◽  
Electron Spectroscopic Imaging ◽  
Dna Backbone ◽  
Two Parameters ◽  
High Level

A multisubunit RNA polymerase enzyme is ultimately responsible for transcription initiation and elongation of RNA, but recognition of the proper start site by the enzyme is regulated by general, temporal and gene-specific trans-factors interacting at promoter and enhancer DNA sequences. To understand the molecular mechanisms which precisely regulate the transcription initiation event, it is crucial to elucidate the structure of the transcription factor/DNA complexes involved. Electron spectroscopic imaging (ESI) provides the opportunity to visualize individual DNA molecules. Enhancement of DNA contrast with ESI is accomplished by imaging with electrons that have interacted with inner shell electrons of phosphorus in the DNA backbone. Phosphorus detection at this intermediately high level of resolution (≈lnm) permits selective imaging of the DNA, to determine whether the protein factors compact, bend or wrap the DNA. Simultaneously, mass analysis and phosphorus content can be measured quantitatively, using adjacent DNA or tobacco mosaic virus (TMV) as mass and phosphorus standards. These two parameters provide stoichiometric information relating the ratios of protein:DNA content.

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