Roundabout is required in the visceral mesoderm for proper microvillus length in the hindgut epithelium

In Drosophila as well as many vertebrate systems, germ cells form extraembryonically and migrate into the embryo before navigating toward gonadal mesodermal cells. How the gonadal mesoderm attracts migratory germ cells is not understood in any system. We have taken a genetic approach to identify genes required for germ cell migration in Drosophila. Here we describe the role of zfh-1 in germ cell migration to the gonadal mesoderm. In zfh-1 mutant embryos, the initial association of germ cells and gonadal mesoderm is blocked. Loss of zfh-1 activity disrupts the development of two distinct mesodermal populations: the caudal visceral mesoderm and the gonadal mesoderm. We demonstrate that the caudal visceral mesoderm facilitates the migration of germ cells from the endoderm to the mesoderm. Zfh-1 is also expressed in the gonadal mesoderm throughout the development of this tissue. Ectopic expression of Zfh-1 is sufficient to induce additional gonadal mesodermal cells and to alter the temporal course of gene expression within these cells. Finally, through analysis of a tinman zfh-1 double mutant, we show that zfh-1 acts in conjunction with tinman, another homeodomain protein, in the specification of lateral mesodermal derivatives, including the gonadal mesoderm.

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The mutant not enough muscles (nem) reveals reduction of the Drosophila embryonic muscle pattern

Journal of Cell Science ◽

10.1242/jcs.108.4.1443 ◽

1995 ◽

Vol 108 (4) ◽

pp. 1443-1454 ◽

Cited By ~ 7

Author(s):

S. Burchard ◽

A. Paululat ◽

U. Hinz ◽

R. Renkawitz-Pohl

Keyword(s):

Myosin Heavy Chain ◽

Heavy Chain ◽

Muscle Development ◽

P Element ◽

Dual Function ◽

Methane Sulfonate ◽

Visceral Mesoderm ◽

Embryonic Muscle ◽

Embryonic Muscle Development ◽

Somatic Musculature

In a search for mutations affecting embryonic muscle development in Drosophila we identified a mutation caused by the insertion of a P-element, which we called not enough muscles (nem). The phenotype of the P-element mutation of the nem gene suggests that it may be required for the development of the somatic musculature and the chordotonal organs of the PNS, while it is not involved in the development of the visceral mesoderm and the dorsal vessel. Mutant embryos are characterized by partial absence of muscles, monitored by immunostainings with mesoderm-specific anti-beta 3 tubulin and anti-myosin heavy chain antibodies. Besides these muscle distortions, defects in the peripheral nervous system were found, indicating a dual function of the nem gene product. Ethyl methane sulfonate-induced alleles for the P-element mutation were created for a detailed analysis. One of these alleles is characterized by unfused myoblasts which express beta 3 tubulin and myosin heavy chain, indicating the state of cell differentiation.

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The gene tinman is required for specification of the heart and visceral muscles in Drosophila

Development ◽

10.1242/dev.118.3.719 ◽

1993 ◽

Vol 118 (3) ◽

pp. 719-729 ◽

Cited By ~ 103

Author(s):

R. Bodmer

Keyword(s):

Heart Development ◽

Body Wall ◽

Heart Cells ◽

Visceral Muscle ◽

Visceral Mesoderm ◽

Body Wall Muscles ◽

Visceral Muscles

The homeobox-containing gene tinman (msh-2, Bodmer et al., 1990 Development 110, 661–669) is expressed in the mesoderm primordium, and this expression requires the function of the mesoderm determinant twist. Later in development, as the first mesodermal subdivisions are occurring, expression becomes limited to the visceral mesoderm and the heart. Here, I show that the function of tinman is required for visceral muscle and heart development. Embryos that are mutant for the tinman gene lack the appearance of visceral mesoderm and of heart primordia, and the fusion of the anterior and posterior endoderm is impaired. Even though tinman mutant embryos do not have a heart or visceral muscles, many of the somatic body wall muscles appear to develop although abnormally. When the tinman cDNA is ubiquitously expressed in tinman mutant embryos, via a heatshock promoter, formation of heart cells and visceral mesoderm is partially restored, tinman seems to be one of the earliest genes required for heart development and the first gene reported for which a crucial function in the early mesodermal subdivisions has been implicated.

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Homeotic genes have specific functional roles in the establishment of the Drosophila embryonic peripheral nervous system

Development ◽

10.1242/dev.115.1.35 ◽

1992 ◽

Vol 115 (1) ◽

pp. 35-47 ◽

Cited By ~ 8

Author(s):

J.G. Heuer ◽

T.C. Kaufman

Keyword(s):

Nervous System ◽

Peripheral Nervous System ◽

Spatial Patterns ◽

Ectopic Expression ◽

Homeotic Genes ◽

Sensory Organs ◽

Sex Combs Reduced ◽

Functional Roles ◽

Visceral Mesoderm ◽

Control Segment

The Drosophila embryonic peripheral nervous system (PNS) contains segment-specific spatial patterns of sensory organs which derive from the ectoderm. Many studies have established that the homeotic genes of Drosophila control segment specific characteristics of the epidermis, and more recently these genes have also been shown to control gut morphogenesis through their expression in the visceral mesoderm (Tremml, G. and Bienz, M. (1989), EMBO J. 8, 2677–2685). We report here the roles of homeotic genes in establishing the spatial patterns of sensory organs in the embryonic PNS. The PNS was examined in embryos homozygous for mutations in the homeotic genes Sex combs reduced (Scr), Antennapedia (Antp), Ultrabithorax (Ubx), abdominal-A (abd-A) and Abdominal-B (Abd-B) with antibodies that label specific subsets of sensory organs. Our results suggest that the homeotic genes have specific roles in establishing the correct spatial patterns of sensory organs in their normal domains of expression. In addition, we also report the effects of ectopic expression of the homeotic genes labial (lab), Deformed (Dfd), Scr, Antp or Ubx on the normal development of sensory organs in the embryonic PNS. Interestingly, while previous studies have concluded that ectopic expression of the homeotic genes Dfd, Scr and Antp has no effect on the segmental identity of the abdominal segments, our results demonstrate that this is not true. We show that ectopic expression of these genes does result in the disruption of the developing PNS in the abdomen. Our results are suggestive of a role for the homeotic gene products in regulating genes which are necessary for generating sensory progenitor cells in the developing PNS.

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decapentaplegic is a direct target of dTcf repression in the Drosophila visceral mesoderm

Development ◽

10.1242/dev.127.17.3695 ◽

2000 ◽

Vol 127 (17) ◽

pp. 3695-3702 ◽

Cited By ~ 1

Author(s):

X. Yang ◽

M. van Beest ◽

H. Clevers ◽

T. Jones ◽

D.A. Hursh ◽

...

Keyword(s):

Gene Expression ◽

Reporter Gene ◽

Transforming Growth Factor Beta ◽

Transcriptional Activation ◽

Binding Sites ◽

Transforming Growth Factor ◽

Ectopic Expression ◽

Reporter Gene Expression ◽

Enhancer Element ◽

Visceral Mesoderm

Drosophila T cell factor (dTcf) mediates transcriptional activation in the presence of Wingless signalling and repression in its absence. Wingless signalling is required for the correct expression of decapentaplegic (dpp), a Transforming Growth Factor (beta) family member, in parasegments 3 and 7 of the Drosophila visceral mesoderm. Here we demonstrate that a dpp enhancer element, which directs expression of a reporter gene in the visceral mesoderm in a pattern indistinguishable from dpp, has two functional dTcf binding sites. Mutations that reduce or eliminate Wingless signalling abolish dpp reporter gene expression in parasegment 3 and reduce it in parasegment 7 while ectopic expression of Wingless signalling components expand reporter gene expression anteriorly in the visceral mesoderm. However, mutation of the dTcf binding sites in the dpp enhancer results in ectopic expression of reporter gene expression throughout the visceral mesoderm, with no diminution of expression in the endogenous sites of expression. These results demonstrate that the primary function of dTcf binding to the dpp enhancer is repression throughout the visceral mesoderm and that activation by Wingless signalling is probably not mediated via these dTcf binding sites to facilitate correct dpp expression in the visceral mesoderm.

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Regulation of the twist target gene tinman by modular cis-regulatory elements during early mesoderm development

Development ◽

10.1242/dev.124.24.4971 ◽

1997 ◽

Vol 124 (24) ◽

pp. 4971-4982 ◽

Cited By ~ 12

Author(s):

Z. Yin ◽

X.L. Xu ◽

M. Frasch

Keyword(s):

Homeobox Gene ◽

Regulatory Elements ◽

Bhlh Protein ◽

Expression Domain ◽

Enhancer Activity ◽

Enhancer Element ◽

Mesoderm Development ◽

Visceral Mesoderm

The Drosophila tinman homeobox gene has a major role in early mesoderm patterning and determines the formation of visceral mesoderm, heart progenitors, specific somatic muscle precursors and glia-like mesodermal cells. These functions of tinman are reflected in its dynamic pattern of expression, which is characterized by initial widespread expression in the trunk mesoderm, then refinement to a broad dorsal mesodermal domain, and finally restricted expression in heart progenitors. Here we show that each of these phases of expression is driven by a discrete enhancer element, the first being active in the early mesoderm, the second in the dorsal mesoderm and the third in cardioblasts. We provide evidence that the early-active enhancer element is a direct target of twist, a gene encoding a basic helix-loop-helix (bHLH) protein, which is necessary for tinman activation. This 180 bp enhancer includes three E-box sequences which bind Twist protein in vitro and are essential for enhancer activity in vivo. Ectodermal misexpression of twist causes ectopic activation of this enhancer in ectodermal cells, indicating that twist is the only mesoderm-specific activator of early tinman expression. We further show that the 180 bp enhancer also includes negatively acting sequences. Binding of Even-skipped to these sequences appears to reduce twist-dependent activation in a periodic fashion, thus producing a striped tinman pattern in the early mesoderm. In addition, these sequences prevent activation of tinman by twist in a defined portion of the head mesoderm that gives rise to hemocytes. We find that this repression requires the function of buttonhead, a head-patterning gene, and that buttonhead is necessary for normal activation of the hematopoietic differentiation gene serpent in the same area. Together, our results show that tinman is controlled by an array of discrete enhancer elements that are activated successively by differential genetic inputs, as well as by closely linked activator and repressor binding sites within an early-acting enhancer, which restrict twist activity to specific areas within the twist expression domain.

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

Development ◽

10.1242/dev.094466 ◽

2013 ◽

Vol 140 (15) ◽

pp. 3156-3166 ◽

Cited By ~ 11

Author(s):

D. Popichenko ◽

F. Hugosson ◽

C. Sjogren ◽

M. Dogru ◽

Y. Yamazaki ◽

...

Keyword(s):

Transcription Factor ◽

Visceral Mesoderm ◽

Lame Duck

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Drosophila myoblast city Encodes a Conserved Protein That Is Essential for Myoblast Fusion, Dorsal Closure, and Cytoskeletal Organization

The Journal of Cell Biology ◽

10.1083/jcb.138.3.589 ◽

1997 ◽

Vol 138 (3) ◽

pp. 589-603 ◽

Cited By ~ 188

Author(s):

Mary Ruth S. Erickson ◽

Brian J. Galletta ◽

Susan M. Abmayr

Keyword(s):

Signal Transduction ◽

Signal Transduction Pathway ◽

Focal Adhesions ◽

Myoblast Fusion ◽

Dorsal Closure ◽

Cytoskeletal Organization ◽

Visceral Mesoderm ◽

Isolation And Characterization ◽

Pole Cells

The Drosophila myoblast city (mbc) locus was previously identified on the basis of a defect in myoblast fusion (Rushton et al., 1995. Development [Camb.]. 121:1979–1988). We describe herein the isolation and characterization of the mbc gene. The mbc transcript and its encoded protein are expressed in a broad range of tissues, including somatic myoblasts, cardial cells, and visceral mesoderm. It is also expressed in the pole cells and in ectodermally derived tissues, including the epidermis. Consistent with this latter expression, mbc mutant embryos exhibit defects in dorsal closure and cytoskeletal organization in the migrating epidermis. Both the mesodermal and ectodermal defects are reminiscent of those induced by altered forms of Drac1 and suggest that mbc may function in the same pathway. MBC bears striking homology to human DOCK180, which interacts with the SH2-SH3 adapter protein Crk and may play a role in signal transduction from focal adhesions. Taken together, these results suggest the possibility that MBC is an intermediate in a signal transduction pathway from the rho/rac family of GTPases to events in the cytoskeleton and that this pathway may be used during myoblast fusion and dorsal closure.

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