Segment polarity gene interactions modulate epidermal patterning in Drosophila embryos

Development ◽  
1993 ◽  
Vol 119 (2) ◽  
pp. 501-517 ◽  
Author(s):  
A. Bejsovec ◽  
E. Wieschaus
Keyword(s):  
Cell Types ◽  
Epidermal Cells ◽  
Specific Cell ◽  
Wild Type ◽  
Individual Gene ◽  
Segment Polarity Genes ◽  
Segment Polarity ◽  
Drosophila Larva ◽  
Cuticular Structures ◽  
Drosophila Embryos

Each segment of a Drosophila larva shows a precisely organized pattern of cuticular structures, indicating diverse cellular identities in the underlying epidermis. Mutations in the segment polarity genes alter the cuticle pattern secreted by the epidermal cells; these mutant patterns provide clues about the role that each gene product plays in the development of wild-type epidermal pattern. We have analyzed embryos that are multiply mutant for five key patterning genes: wingless, patched, engrailed, naked and hedgehog. Our results indicate that wild-type activity of these five segment polarity genes can account for most of the ventral pattern elements and that their gene products interact extensively to specify the diverse cellular identities within the epidermis. Two pattern elements can be correlated with individual gene action: wingless is required for formation of naked cuticle and engrailed is required for formation of the first row of denticles in each abdominal denticle belt. The remaining cell types can be produced by different combinations of the five gene activities. wingless activity generates the diversity of cell types within the segment, but each specific cell identity depends on the activity of patched, engrailed, naked and hedgehog. These molecules modulate the distribution and interpretation of wingless signalling activity in the ventral epidermal cells and, in addition, each can contribute to pattern through a pathway independent of the wingless signalling pathway.

Pituitary ontogeny of the Snell dwarf mouse reveals Pit-1-independent and Pit-1-dependent origins of the thyrotrope

Development ◽  
1994 ◽  
Vol 120 (3) ◽  
pp. 515-522 ◽  
Author(s):  
S.C. Lin ◽  
S. Li ◽  
D.W. Drolet ◽  
M.G. Rosenfeld
Keyword(s):  
Molecular Mechanisms ◽  
Cell Types ◽  
Cell Phenotype ◽  
Specific Cell ◽  
Mutant Form ◽  
Wild Type ◽  
Pou Domain ◽  
Distinct Cell ◽  
Snell Dwarf ◽  
Dwarf Mice

The anterior pituitary provides a model to study the molecular mechanisms responsible for emergence of distinct cell types within an organ. Dwarf mice (Snell) that express a mutant form of the tissue-specific POU-domain transcription factor Pit-1 fail to generate three cell types, including the thyrotrope (S. Li, E. B. Crenshaw, E. J. Rawson, D. S. Simmons, L. Swanson and M. G. Rosenfeld (1990), Nature 347, 528–533). Analyses of wild-type and Pit-1-defective mice, presented here, have revealed that thyrotropes unexpectedly arise from two independent cell populations. The first population is Pit-1-independent and appears on e12 in the rostral tip of the developing gland, but phenotypically disappears by the day of birth. The second is Pit-1-dependent and arises subsequently in the caudomedial portion of the developing gland (e15.5), following the initial expression of Pit-1 in this region. The failure of caudomedial thyrotrope cells to appear in the Snell dwarf, and the observation that Pit-1 can bind to and transactivate the TSH beta promoter, apparently enhanced by its phosphorylation, suggests that Pit-1 is directly required for the appearance of this distinct population that serves as the precursors of the mature thyrotrope cell type. These data suggest that different molecular mechanisms, based on the actions of distinct transcription factors, can serve to independently generate a specific cell phenotype during mammalian organogenesis.

Subcellular localization of the segment polarity protein patched suggests an interaction with the wingless reception complex in Drosophila embryos

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 987-998 ◽  
Author(s):  
J. Capdevila ◽  
F. Pariente ◽  
J. Sampedro ◽  
J.L. Alonso ◽  
I. Guerrero
Keyword(s):  
Transmembrane Protein ◽  
Cell Communication ◽  
Epidermal Cells ◽  
Communication Processes ◽  
Segment Polarity ◽  
Membrane Bound ◽  
Endocytic Vesicles ◽  
Segment Polarity Gene ◽  
Drosophila Embryos ◽  
Polarity Gene

The product of the segment polarity gene patched is a transmembrane protein involved in the cell communication processes that establish polarity within the embryonic segments of Drosophila. Monoclonal antibodies have been raised against the patched protein, and by immunoelectron microscopy part of the patched staining is found associated with discrete regions of the lateral plasma membrane of the embryonic epidermal cells. Using a mutation affecting endocytosis (shibire) we find that patched is a membrane-bound protein, which is internalized by endocytosis, and that the preferential sites of accumulation resemble the described localization of the cell-cell adhesive junctions of the epidermal cells. patched partially co-localizes with the wingless protein in the wingless-expressing and nearby cells, in structures that seem to be endocytic vesicles. These data suggest the interaction of patched protein with elements of the reception complex of wingless, as a way to control the wingless expression.

Abstract 517: Effect of Hepatocyte-specific Depletion of AT1a Receptors on Atherosclerosis and Aneurysms

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Debra L Rateri ◽  
Anju Balakrishnan ◽  
Deborah A Howatt ◽  
Jessica J Moorleghen ◽  
Lisa A Cassis ◽  
...  
Keyword(s):  
Saturated Fat ◽  
Cell Types ◽  
Aortic Aneurysms ◽  
Vascular Pathology ◽  
Whole Body ◽  
Similar Degree ◽  
Specific Cell ◽  
Wild Type ◽  
Atherosclerotic Burden ◽  
Blood Pressures

Background and Objective Whole body deficiency of AT1a receptors (AT1aRs) ablates angiotensin II (AngII) induced vascular pathologies that include aortic aneurysms and atherosclerosis. We created AT1aR floxed mice to determine the role of specific cell types expressing this receptor on these vascular pathologies. Unexpectedly, these mice demonstrated a lack of effect of smooth muscle specific AT1aR deficiency on the development of atherosclerosis or aneurysms. Also, endothelial-specific AT1aR deficiency had no effect in atherosclerosis and minimal effect on aneurysms. The purpose of this study was to determined if AngII infusion was releasing substances from the liver that influence vascular pathology. Methods and Results Hepatocyte depletion of AT1aRs was accomplished using two methods of introducing Cre into AT1aR floxed mice. One approach was injection of adenovirus Cre (AdCre) and the other by breeding to mice expressing Cre under the control of the albumin promoter. To induce atherosclerosis, groups of wild type and hepatocyte-specific AT1aR depleted male (N=15-21/group) and female (N=21/group) mice were fed a saturated fat enriched diet for 12 weeks. Hepatocyte-specific depletion of AT1aRs was confirmed using detection of Cre and absence of AT1aRs by PCR and RT-PCR, respectively. Body weights, serum cholesterol concentrations, and systemic blood pressures were not different between wild type and hepatocyte-specific AT1aR depleted mice grouped by gender and genotype. Atherosclerotic burden was similar in all groups. To examine AngII-induced atherosclerosis, male wild type and hepatocyte-specific AT1aR depleted mice (N=11-16/group) were fed a fat enriched diet for 5 weeks, and AngII (1,000 mg/kg/min) was infused using osmotic mini-pumps for 28 days. AngII infusion increased systolic blood pressure, promoted atherosclerosis and induced aneurysms to a similar degree in both genotypes. Conclusion Deletion of hepatocyte-specific AT1aRs did not affect dietary or AngII-induced vascular pathologies.

Imaginal discs can be recovered from cultured embryos mutant for the segment-polarity genes engrailed, naked and patched but not from wingless

Development ◽  
1989 ◽  
Vol 107 (4) ◽  
pp. 715-722 ◽  
Author(s):  
A.A. Simcox ◽  
I.J.H. Roberts ◽  
E. Hersperger ◽  
M.C. Gribbin ◽  
A. Shearn ◽  
...  
Keyword(s):  
Imaginal Discs ◽  
Larval Cuticle ◽  
Segment Polarity Genes ◽  
Abnormal Morphology ◽  
In Vivo Culture ◽  
Segment Polarity ◽  
Abnormal Pattern ◽  
Drosophila Embryos

Drosophila embryos homozygous for strong mutations in each of the segment-polarity genes wingless (wg), engrailed (en), naked (nkd) and patched (ptc) form a larval cuticle in which there is a deletion in every segment. The mutant embryos normally fail to hatch but by in vivo culture we were able to show which could produce adult structures. Cultured wg- embryos did not produce any adult structures. Cultured en- embryos produced eye-antennal derivatives and rarely produced partial thoracic structures. nkd- and ptc- embryos produced eye-antennal and thoracic derivatives. The nkd- and ptc- thoracic imaginal discs developed with an abnormal morphology and abnormal pattern of en- expression. Our findings are consistent with the idea that the thoracic imaginal discs derive from two adjacent groups of cells that express wg and en respectively in the embryo.

scholarly journals High-resolution contrast-enhanced microCT reveals the true three-dimensional morphology of the murine placenta

2019 ◽  
Vol 116 (28) ◽  
pp. 13927-13936 ◽  
Author(s):  
Katrien De Clercq ◽  
Eleonora Persoons ◽  
Tina Napso ◽  
Catherine Luyten ◽  
Tatjana N. Parac-Vogt ◽  
...  
Keyword(s):  
High Resolution ◽  
Volume Fraction ◽  
Three Dimensional ◽  
Cell Types ◽  
Mouse Strains ◽  
Specific Cell ◽  
Placental Development ◽  
Individual Gene ◽  
Contrast Enhanced ◽  
Late Stages

Genetic engineering of the mouse genome identified many genes that are essential for embryogenesis. Remarkably, the prevalence of concomitant placental defects in embryonic lethal mutants is highly underestimated and indicates the importance of detailed placental analysis when phenotyping new individual gene knockouts. Here we introduce high-resolution contrast-enhanced microfocus computed tomography (CE-CT) as a nondestructive, high-throughput technique to evaluate the 3D placental morphology. Using a contrast agent, zirconium-substituted Keggin polyoxometalate (Zr-POM), the soft tissue of the placenta (i.e., different layers and cell types and its vasculature) was imaged with a resolution of 3.5 µm voxel size. This approach allowed us to visualize and study early and late stages of placental development. Moreover, CE-CT provides a method to precisely quantify placental parameters (i.e., volumes, volume fraction, ratio of different placental layers, and volumes of specific cell populations) that are crucial for statistical comparison studies. The CE-CT assessment of the 3D morphology of the placentas was validated (i) by comparison with standard histological studies; (ii) by evaluating placentas from 2 different mouse strains, 129S6 and C57BL/6J mice; and (iii) by confirming the placental phenotype of mice lacking phosphoinositol 3-kinase (PI3K)-p110α. Finally, the Zr-POM–based CE-CT allowed for inspection of the vasculature structure in the entire placenta, as well as detecting placental defects in pathologies characterized by embryonic resorption and placental fusion. Taken together, Zr-POM–based CE-CT offers a quantitative 3D methodology to investigate placental development or pathologies.

Patterned epidermal cell death in wild-type and segment polarity mutant Drosophila embryos

Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3427-3436 ◽  
Author(s):  
T.M. Pazdera ◽  
P. Janardhan ◽  
J.S. Minden
Keyword(s):  
Cell Death ◽  
Embryonic Development ◽  
Epidermal Cell ◽  
Time Lapse ◽  
Wild Type ◽  
Segment Polarity ◽  
Genetic Perturbations ◽  
Mutant Phenotypes ◽  
Cell Death Pattern ◽  
Drosophila Embryos

Programmed cell death plays an essential role in the normal embryonic development of Drosophila melanogaster. One region of the embryo where cell death occurs, but has not been studied in detail, is the abdominal epidermis. Because cell death is a fleeting process, we have used time-lapse, fluorescence microscopy to map epidermal apoptosis throughout embryonic development. Cell death occurs in a stereotypically striped pattern near both sides of the segment border and to a lesser extent in the middle of the segment. This map of wild-type cell death was used to determine how cell death patterns change in response to genetic perturbations that affect epidermal patterning. Previous studies have suggested that segment polarity mutant phenotypes are partially the result of increased cell death. Mutations in wingless, armadillo, and gooseberry led to dramatic increases in apoptosis in the anterior of the segment while a naked mutation resulted in a dramatic increase in the death of engrailed cells in the posterior of the segment. These results show that segment polarity gene expression is necessary for the survival of specific rows of epidermal cells and may provide insight into the establishment of the wild-type epidermal cell death pattern.

Cell culture of individual Drosophila embryos

Development ◽  
1978 ◽  
Vol 45 (1) ◽  
pp. 161-172
Author(s):  
David P. Cross ◽  
James H. Sang
Keyword(s):  
Fat Body ◽  
Individual Cell ◽  
Cell Types ◽  
Wild Type ◽  
Initial Appearance ◽  
Developmental Capacity ◽  
In Vitro Cell Cultures ◽  
Nerve Muscle ◽  
Drosophila Embryos

A new procedure is described for the preparation of in vitro cell cultures from individual early gastrulae of Drosophila melanogaster. In these cultures several identifiable cell types differentiate within 24 h (nerve, muscle, fat-body, haemocyte and chitin-secreting): their initial appearance and continuing development over a period of weeks is described. It is proposed that this technique may be used to analyse abnormalities of cellular development in embryonic lethal mutants. Culture in vitro of cells from lethal embryos is seen to have two broad roles: (1) to test the developmental capacity of individual cell types in a situation where they are relatively free from possible deleterious interactions with other cell types and are liberated from the system of the dying embryo, and (2) through the preparation of mixed cultures from normal and mutant embryos, to determine the influence of the presence of wild-type cells on observed abnormalities of a particular cell type.

puckered, a gene involved in position-specific cell differentiation in the dorsal epidermis of the Drosophila larva

Development ◽  
1993 ◽  
Vol 119 (Supplement) ◽  
pp. 251-259 ◽  
Author(s):  
J. M. Ring ◽  
A. Martinez Arias
Keyword(s):  
Cell Differentiation ◽  
Relative Position ◽  
Positional Information ◽  
Epidermal Cells ◽  
Cell Interactions ◽  
Specific Cell ◽  
Specific Behaviour ◽  
Drosophila Larva ◽  
To Receive ◽  
Dorsal Epidermis

The final pattern of the cuticle of the Drosophila larva depends on the position-specific behaviour of the epidermal cells during their differentiation. This behaviour is dictated, in part, by the relative position of the cells during embryogenesis which allows them to receive and integrate signals from their neighbours. The translation of this ‘positional information’ into pattern might depend on the activity of genes that are able to integrate the outcome of cell interactions and tranfer it to the genes responsible for cell differentiation. Mutations in the gene puckered cause spatially restricted defects during the differentiation of the larval epidermal cells. We present data that suggests puckered may be involved in linking positional information to cell differentiation.

Control of segmental asymmetry in Drosophila embryos

Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 785-796 ◽  
Author(s):  
A.S. Manoukian ◽  
H.M. Krause
Keyword(s):  
Double Negative ◽  
Common Theme ◽  
Negative Regulators ◽  
Fushi Tarazu ◽  
Segment Polarity Genes ◽  
Segment Polarity ◽  
Body Patterning ◽  
Blastoderm Stage ◽  
Pair Rule ◽  
Drosophila Embryos

During Drosophila development, an important aspect of body patterning is the division of the embryo into repeating morphological units referred to as parasegments. The parasegmental domains are first defined at the blastoderm stage by alternating stripes of transcripts encoded by the pair-rule genes fushi tarazu (ftz) and even-skipped (eve) and later by stripes encoded by the segment polarity genes engrailed (en) and wingless. Here, we show that the runt gene (run) is required to generate asymmetries within these parasegmental domains. Using a heat-shock-inducible run transgene, we found that ectopic run expression leads to rapid repression of eve stripes and a somewhat delayed expansion of ftz stripes. Unexpectedly, we also found that ectopic run was a rapid and potent repressor of odd-numbered en stripes. Two remarkably different segmental phenotypes were generated as a consequence of these effects. In solving the mechanisms underlying these phenotypes, we discovered that the positioning of en stripes is largely determined by the actions of negative regulators. Our data indicate that run is required to limit the domains of en expression in the odd-numbered parasegments, while the odd-skipped gene is required to limit the domains of en expression in the even-numbered parasegments. Activation of en at the anterior margins of both sets of parasegments requires the repression of run and odd by the product of the eve gene. The spatial restriction of gene expression via negative and double negative pathways such as these is likely to be a common theme during development.

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