Gastrulation in Drosophila: the formation of the ventral furrow and posterior midgut invaginations

Development ◽  
1991 ◽  
Vol 112 (3) ◽  
pp. 775-789 ◽  
Author(s):  
D. Sweeton ◽  
S. Parks ◽  
M. Costa ◽  
E. Wieschaus
Keyword(s):  
Cell Shape ◽  
Time Course ◽  
Drosophila Embryo ◽  
Second Phase ◽  
Rapid Phase ◽  
Apical Constriction ◽  
Posterior Midgut ◽  
Ventral Furrow ◽  
Two Phases ◽  
Shape Changes

The ventral furrow and posterior midgut invaginations bring mesodermal and endodermal precursor cells into the interior of the Drosophila embryo during gastrulation. Both invaginations proceed through a similar sequence of rapid cell shape changes, which include apical flattening, constriction of the apical diameter, cell elongation and subsequent shortening. Based on the time course of apical constriction in the ventral furrow and posterior midgut, we identify two phases in this process: first, a slow stochastic phase in which some individual cells begin to constrict and, second, a rapid phase in which the remaining unconstricted cells constrict. Mutations in the concertina or folded gastrulation genes appear to block the transition to the second phase in both the ventral furrow and the posterior midgut invaginations.

Drosophila gastrulation: analysis of cell shape changes in living embryos by three-dimensional fluorescence microscopy

Development ◽  
1991 ◽  
Vol 112 (2) ◽  
pp. 365-370 ◽  
Author(s):  
Z. Kam ◽  
J.S. Minden ◽  
D.A. Agard ◽  
J.W. Sedat ◽  
M. Leptin
Keyword(s):  
Cell Shape ◽  
Three Dimensional ◽  
Time Lapse ◽  
Second Phase ◽  
Fluorescent Markers ◽  
Ventral Furrow ◽  
Cell Shapes ◽  
Cell Shape Changes ◽  
Two Phases ◽  
Shape Changes

The first event of Drosophila gastrulation is the formation of the ventral furrow. This process, which leads to the invagination of the mesoderm, is a classical example of epithelial folding. To understand better the cellular changes and dynamics of furrow formation, we examined living Drosophila embryos using three-dimensional time-lapse microscopy. By injecting fluorescent markers that visualize cell outlines and nuclei, we monitored changes in cell shapes and nuclear positions. We find that the ventral furrow invaginates in two phases. During the first ‘preparatory’ phase, many prospective furrow cells in apparently random positions gradually begin to change shape, but the curvature of the epithelium hardly changes. In the second phase, when a critical number of cells have begun to change shape, the furrow suddenly invaginates. Our results suggest that furrow formation does not result from an ordered wave of cell shape changes, contrary to a model for epithelial invagination in which a wave of apical contractions causes invagination. Instead, it appears that cells change their shape independently, in a stochastic manner, and the sum of these individual changes alters the curvature of the whole epithelium.

Cell shape changes during gastrulation in Drosophila

Development ◽  
1990 ◽  
Vol 110 (1) ◽  
pp. 73-84 ◽  
Author(s):  
M. Leptin ◽  
B. Grunewald
Keyword(s):  
Cell Fate ◽  
Cell Shape ◽  
Multilayered Structure ◽  
Second Phase ◽  
Specific Cell ◽  
Ventral Furrow ◽  
Correct Execution ◽  
Cell Shape Changes ◽  
Two Phases ◽  
Shape Changes

The first morphogenetic movement during Drosophila development is the invagination of the mesoderm, an event that folds a one-layered epithelium into a multilayered structure. In this paper, we describe the shape changes and behaviour of the cells participating in this process and show how mutations that change cell fate affect this behaviour. We divide the formation of the mesodermal germ layer into two phases. During the first phase, the ventral epithelium folds into a tube by a series of concerted cell shape changes (ventral furrow formation). Based on the behaviour of cells in this phase, we conclude that the prospective mesoderm is not a homogeneous cell population, but consists of two subpopulations. Each subpopulation goes through a distinctive sequence of specific cell shape changes which together mediate the invagination of the ventral furrow. In the second phase, the invaginated tube of mesoderm loses its epithelial character, the mesoderm cells disperse, divide and then spread out along the ectoderm to form a single cell layer. To test how ventral furrow formation depends on cell fates in the mesoderm and in neighbouring cells we alter these fates genetically using maternal and zygotic mutations. These experiments show that some of the aspects of cell behaviour specific for ventral furrow cells are part of an autonomous differentiation programme. The force driving the invagination is generated within the region of the ventral furrow, with the lateral and dorsal cell populations contributing little or none of the force. Two known zygotic genes that are required for the formation of the mesoderm, twist and snail, are expressed in ventral furrow cells, and the correct execution of cell shape changes in the mesoderm depends on both. Finally, we show that the region where the ventral furrow forms is determined by the expression of mesoderm-specific genes, and not by mechanical or other epigenetic properties of the egg.

scholarly journals Hyperactivation of the folded gastrulation pathway induces specific cell shape changes

Development ◽  
1998 ◽  
Vol 125 (4) ◽  
pp. 589-597 ◽  
Author(s):  
P. Morize ◽  
A.E. Christiansen ◽  
M. Costa ◽  
S. Parks ◽  
E. Wieschaus
Keyword(s):  
Cell Shape ◽  
Inducible Promoter ◽  
Specific Cell ◽  
Apical Surface ◽  
Apical Constriction ◽  
Cellular Effects ◽  
Ventral Furrow ◽  
Cell Shape Changes ◽  
Shape Changes

During Drosophila gastrulation, mesodermal precursors are brought into the interior of the embryo by formation of the ventral furrow. The first steps of ventral furrow formation involve a flattening of the apical surface of the presumptive mesodermal cells and a constriction of their apical diameters. In embryos mutant for folded gastrulation (fog), these cell shape changes occur but the timing and synchrony of the constrictions are abnormal. A similar phenotype is seen in a maternal effect mutant, concertina (cta). fog encodes a putative secreted protein whereas cta encodes an (alpha)-subunit of a heterotrimeric G protein. We have proposed that localized expression of the fog signaling protein induces apical constriction by interacting with a receptor whose downstream cellular effects are mediated by the cta G(alpha)protein. <P> In order to test this model, we have ectopically expressed fog at the blastoderm stage using an inducible promoter. In addition, we have examined the constitutive activation of cta protein by blocking GTP hydrolysis using both in vitro synthesized mutant alleles and cholera toxin treatment. Activation of the fog/cta pathway by any of these procedures results in ectopic cell shape changes in the gastrula. Uniform fog expression rescues the gastrulation defects of fog null embryos but not cta mutant embryos, arguing that cta functions downstream of fog expression. The normal location of the ventral furrow in embryos with uniformly expressed fog suggests the existence of a fog-independent pathway determining mesoderm-specific cell behaviors and invagination. Epistasis experiments indicate that this pathway requires snail but not twist expression.

Mechanisms of early Drosophila mesoderm formation

Development ◽  
1992 ◽  
Vol 116 (Supplement) ◽  
pp. 23-31 ◽  
Author(s):  
Maria Leptin ◽  
José Casal ◽  
Barbara Grunewald ◽  
Rolf Reuter
Keyword(s):  
Cell Shape ◽  
Cell Populations ◽  
Genetic Screens ◽  
Germ Band ◽  
Posterior Midgut ◽  
Ventral Furrow ◽  
Mesoderm Formation ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Different Parts

Several morphogenetic processes occur simultaneously during Drosophila gastrulation, including ventral furrow invagination to form the mesoderm, anterior and posterior midgut invagination to create the endoderm, and germ band extension. Mutations changing the behaviour of different parts of the embryo can be used to test the roles of different cell populations in gastrulation. Posterior midgut morphogenesis and germ band extension are partly independent, and neither depends on mesoderm formation, nor mesoderm formation on them. The invagination of the ventral furrow is caused by forces from within the prospective mesoderm (i. e. the invaginating cells) without any necessary contribution from other parts of the embryo. The events that lead to the cell shape changes mediating ventral furrow formation require the transcription of zygotic genes under the control of twist and snail. Such genes can be isolated by molecular and genetic screens.

Autonomy and non-autonomy in Drosophila mesoderm determination and morphogenesis

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 853-859 ◽  
Author(s):  
M. Leptin ◽  
S. Roth
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Developmental Program ◽  
Cell Shape Change ◽  
Ventral Furrow ◽  
Large Numbers ◽  
The Individual ◽  
Mutant Cells ◽  
Transplantation Experiments ◽  
Shape Changes

The mesoderm in Drosophila invaginates by a series of characteristic cell shape changes. Mosaics of wild-type cells in an environment of mutant cells incapable of making mesodermal invaginations show that this morphogenetic behaviour does not require interactions between large numbers of cells but that small patches of cells can invaginate independent of their neighbours' behaviour. While the initiation of cell shape change is locally autonomous, the shapes the cells assume are partly determined by the individual cell's environment. Cytoplasmic transplantation experiments show that areas of cells expressing mesodermal genes ectopically at any position in the egg form an invagination. We propose that ventral furrow formation is the consequence of all prospective mesodermal cells independently following their developmental program. Gene expression at the border of the mesoderm is induced by the apposition of mesodermal and non-mesodermal cells.

scholarly journals Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division

2019 ◽  
Author(s):  
Clint S. Ko ◽  
Prateek Kalakuntla ◽  
Adam C. Martin
Keyword(s):  
Cell Division ◽  
Cell Shape ◽  
Mitotic Cell ◽  
Signal Interference ◽  
Apical Constriction ◽  
Mitotic Entry ◽  
Cell Divisions ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Mitotic Cells

AbstractDuring development, coordinated cell shape changes and cell divisions sculpt tissues. While these individual cell behaviors have been extensively studied, how cell shape changes and cell divisions that occur concurrently in epithelia influence tissue shape is less understood. We addressed this question in two contexts of the early Drosophila embryo: premature cell division during mesoderm invagination, and native ectodermal cell divisions with ectopic activation of apical contractility. Using quantitative live-cell imaging, we demonstrated that mitotic entry reverses apical contractility by interfering with medioapical RhoA signaling. While premature mitotic entry inhibits mesoderm invagination, which relies on apical constriction, mitotic entry in an artificially contractile ectoderm induced ectopic tissue invaginations. Ectopic invaginations resulted from medioapical myosin loss in neighboring mitotic cells. This myosin loss enabled non-mitotic cells to apically constrict through mitotic cell stretching. Thus, the spatial pattern of mitotic entry can differentially regulate tissue shape through signal interference between apical contractility and mitosis.

scholarly journals New kinetic analysis of the Fenton reaction: Critical examination of the free radical – chain reaction concept

2019 ◽  
Vol 44 (4) ◽  
pp. 289-299
Author(s):  
Mordechai L Kremer
Keyword(s):  
Free Radical ◽  
Fenton Reaction ◽  
Critical Examination ◽  
Complete Agreement ◽  
Time Interval ◽  
Second Phase ◽  
Chain Reaction ◽  
Rapid Phase ◽  
Two Phases ◽  
Radical Model

Using [H2O2] in the molar range, the reaction with Fe2+ has two phases: in the first rapid phase, only a small fraction of the total O2 is evolved; the bulk of the gas is formed in a slow second phase. In interpretations based on the free radical model of Barb et al., the first phase has been identified with the ‘Fenton reaction’ (reaction of Fe2+with H2O2), while the second with catalytic decomposition of H2O2 by Fe3+ ions. This interpretation is not correct. A new analysis of the model shows that (1) it is a chain reaction having no termination steps and (2) the ‘Fenton part’ alone consists of two phases. It starts with rapid evolution of O2 via a five-membered chain reaction (first phase). When [Fe2+] becomes low, evolution of O2 continues in a three-membered chain reaction at a greatly reduced rate (second phase). In later stages of the second phase, Fe3+ catalysis contributes to O2 evolution. Thus, the amount of O2 formed in the rapid phase cannot be identified with the total amount formed in the ‘Fenton reaction’ but only with that formed in its first phase. Computer simulations of O2 evolution based on the model of Barb et al. and rate constants show a definite dependence of this quantity on the initial [H2O2] – in contrast to the experimentally found independence. More satisfactory, but not complete, agreement with measured data could be reached in simulations using a non-radical model. Some of the difficulty has been due to the determination of the exact position of the end of the first phase. The transition between the two phases of the reaction occurs in a short, but finite time interval. It has been shown that the quantity ‘total amount of O2 evolved in the Fenton reaction’ (subtracting the part due to Fe3+catalysis) is not accessible to experimental determination nor to theoretical calculation.

Uptake of leucine by Chlorella symbionts of green hydra

1988 ◽  
Vol 234 (1276) ◽  
pp. 319-332 ◽  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Time Course ◽  
Algal Cell ◽  
Short Interval ◽  
Artemia Salina ◽  
Second Phase ◽  
Rapid Phase ◽  
Green Hydra ◽  
The Difference

Cells of a Chlorella sp. symbiotic with green hydra were able to take up leucine via a high-affinity transport mechanism after isolation from the symbiosis, and to incorporate sequestered amino acid into protein. The time course of uptake of leucine by Chlorella cells in the intact symbiosis was followed after hydra were fed with nauplii of the brine shrimp Artemia salina that had been labelled with radioactive leucine. Uptake proceeded in two stages, the first more rapid than the second, separated by a short interval in which there was a consistently observed decrease in the amount of radioactivity per cell. Although leucine from Artemia free amino acid pools was accumulated disproportionately by Chlorella cells in symbiosis, this was not sufficient to explain the initial rapid phase of uptake, nor could changes in rate of uptake with time after feeding be explained by changes in properties of the Chlorella cells. Rather, slower uptake in the second phase, and the decrease in amount of radioactivity per cell which preceded it, were probably due to changes in supply of amino acids to the Chlorella cells. Amino acids transported by the same system as leucine caused efflux of accumulated leucine from isolated Chlorella cells when present in high external concentrations. Thus the observed accumulation of radioactivity in symbiosis may have been the difference between unidirectional influx and unidirectional efflux of leucine dependent upon changes in external concentrations of unlabelled amino acids from Artemia or from hydra pools. This is discussed with reference to host control of algal cell division, which has been shown to be dependent upon supply of a ‘division factor’ from host food.

scholarly journals Integrin binding and cell spreading on extracellular matrix act at different points in the cell cycle to promote hepatocyte growth.

1994 ◽  
Vol 5 (9) ◽  
pp. 967-975 ◽  
Author(s):  
L K Hansen ◽  
D J Mooney ◽  
J P Vacanti ◽  
D E Ingber
Keyword(s):  
Cell Cycle ◽  
Extracellular Matrix ◽  
Cell Shape ◽  
Time Course ◽  
Cell Spreading ◽  
S Phase ◽  
Similar Time ◽  
Cell Shape Changes ◽  
Hepatocyte Growth ◽  
Shape Changes

This study was undertaken to determine the importance of integrin binding and cell shape changes in the control of cell-cycle progression by extracellular matrix (ECM). Primary rat hepatocytes were cultured on ECM-coated dishes in serum-free medium with saturating amounts of growth factors (epidermal growth factor and insulin). Integrin binding and cell spreading were promoted in parallel by plating cells on dishes coated with fibronectin (FN). Integrin binding was separated from cell shape changes by culturing cells on dishes coated with a synthetic arg-gly-asp (RGD)-peptide that acts as an integrin ligand but does not support hepatocyte extension. Expression of early (junB) and late (ras) growth response genes and DNA synthesis were measured to determine whether these substrata induce G0-synchronized hepatocytes to reenter the growth cycle. Cells plated on FN exhibited transient increases in junB and ras gene expression (within 2 and 8 h after plating, respectively) and synchronous entry into S phase. Induction of junB and ras was observed over a similar time course in cells on RGD-coated dishes, however, these round cells did not enter S phase. The possibility that round cells on RGD were blocked in mid to late G1 was confirmed by the finding that when trypsinized and replated onto FN-coated dishes after 30 h of culture, they required a similar time (12-15 h) to reenter S phase as cells that had been spread and allowed to progress through G1 on FN. We have previously shown that hepatocytes remain viable and maintain high levels of liver-specific functions when cultured on these RGD-coated dishes. Thus, these results suggest that ECM acts at two different points in the cell cycle to regulate hepatocyte growth: first, by activating the G0/G1 transition via integrin binding and second, by promoting the G1/S phase transition and switching off the default differentiation program through mechanisms related to cell spreading.

scholarly journals DRhoGEF2 and Diaphanous Regulate Contractile Force during Segmental Groove Morphogenesis in the Drosophila Embryo

2008 ◽  
Vol 19 (5) ◽  
pp. 1883-1892 ◽  
Author(s):  
Shai Mulinari ◽  
Mojgan Padash Barmchi ◽  
Udo Häcker
Keyword(s):  
Cell Shape ◽  
Cell Formation ◽  
Small Gtpases ◽  
Cell Junctions ◽  
Drosophila Embryo ◽  
Cell Cortex ◽  
Nucleotide Exchange ◽  
Apical Constriction ◽  
Guanine Nucleotide Exchange ◽  
Nucleotide Exchange Factors

Morphogenesis of the Drosophila embryo is associated with dynamic rearrangement of the actin cytoskeleton mediated by small GTPases of the Rho family. These GTPases act as molecular switches that are activated by guanine nucleotide exchange factors. One of these factors, DRhoGEF2, plays an important role in the constriction of actin filaments during pole cell formation, blastoderm cellularization, and invagination of the germ layers. Here, we show that DRhoGEF2 is equally important during morphogenesis of segmental grooves, which become apparent as tissue infoldings during mid-embryogenesis. Examination of DRhoGEF2-mutant embryos indicates a role for DRhoGEF2 in the control of cell shape changes during segmental groove morphogenesis. Overexpression of DRhoGEF2 in the ectoderm recruits myosin II to the cell cortex and induces cell contraction. At groove regression, DRhoGEF2 is enriched in cells posterior to the groove that undergo apical constriction, indicating that groove regression is an active process. We further show that the Formin Diaphanous is required for groove formation and strengthens cell junctions in the epidermis. Morphological analysis suggests that Dia regulates cell shape in a way distinct from DRhoGEF2. We propose that DRhoGEF2 acts through Rho1 to regulate acto-myosin constriction but not Diaphanous-mediated F-actin nucleation during segmental groove morphogenesis.

Sign in / Sign up

Export Citation Format

Share Document