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.

Second-Site Noncomplementation Identifies Genomic Regions Required for Drosophila Nonmuscle Myosin Function During Morphogenesis

Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1845-1863
Author(s):  
Susan R Halsell ◽  
Daniel P Kiehart
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Nonmuscle Myosin ◽  
Genetic Screens ◽  
Nonmuscle Myosin Ii ◽  
Cell Shape Changes ◽  
Genomic Regions ◽  
Shape Changes ◽  
Strong Interactors

Abstract Drosophila is an ideal metazoan model system for analyzing the role of nonmuscle myosin-II (henceforth, myosin) during development. In Drosophila, myosin function is required for cytokinesis and morphogenesis driven by cell migration and/or cell shape changes during oogenesis, embryogenesis, larval development and pupal metamorphosis. The mechanisms that regulate myosin function and the supramolecular structures into which myosin incorporates have not been systematically characterized. The genetic screens described here identify genomic regions that uncover loci that facilitate myosin function. The nonmuscle myosin heavy chain is encoded by a single locus, zipper. Contiguous chromosomal deficiencies that represent approximately 70% of the euchromatic genome were screened for genetic interactions with two recessive lethal alleles of zipper in a second-site noncomplementation assay for the malformed phenotype. Malformation in the adult leg reflects aberrations in cell shape changes driven by myosin-based contraction during leg morphogenesis. Of the 158 deficiencies tested, 47 behaved as second-site noncomplementors of zipper. Two of the deficiencies are strong interactors, 17 are intermediate and 28 are weak. Finer genetic mapping reveals that mutations in cytoplasmic tropomyosin and viking (collagen IV) behave as second-site noncomplementors of zipper during leg morphogenesis and that zipper function requires a previously uncharacterized locus, E3.10/J3.8, for leg morphogenesis and viability.

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.

scholarly journals Control of germ-band retraction in Drosophila by the zinc-finger protein HINDSIGHT

Development ◽  
1997 ◽  
Vol 124 (11) ◽  
pp. 2129-2141 ◽  
Author(s):  
M.L. Yip ◽  
M.L. Lamka ◽  
H.D. Lipshitz
Keyword(s):  
Cell Shape ◽  
Zinc Finger Protein ◽  
Early Embryo ◽  
Malpighian Tubules ◽  
Chemical Signaling ◽  
Germ Band ◽  
Tracheal System ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Drosophila Embryos

Drosophila embryos lacking hindsight gene function have a normal body plan and undergo normal germ-band extension. However, they fail to retract their germ bands. hindsight encodes a large nuclear protein of 1920 amino acids that contains fourteen C2H2-type zinc fingers, and glutamine-rich and proline-rich domains, suggesting that it functions as a transcription factor. Initial embryonic expression of hindsight RNA and protein occurs in the endoderm (midgut) and extraembryonic membrane (amnioserosa) prior to germ-band extension and continues in these tissues beyond the completion of germ-band retraction. Expression also occurs in the developing tracheal system, central and peripheral nervous systems, and the ureter of the Malpighian tubules. Strikingly, hindsight is not expressed in the epidermal ectoderm which is the tissue that undergoes the cell shape changes and movements during germ-band retraction. The embryonic midgut can be eliminated without affecting germ-band retraction. However, elimination of the amnioserosa results in the failure of germ-band retraction, implicating amnioserosal expression of hindsight as crucial for this process. Ubiquitous expression of hindsight in the early embryo rescues germ-band retraction without producing dominant gain-of-function defects, suggesting that hindsight's role in germ-band retraction is permissive rather than instructive. Previous analyses have shown that hindsight is required for maintenance of the differentiated amnioserosa (Frank, L. C. and Rushlow, C. (1996) Development 122, 1343–1352). Two classes of models are consistent with the present data. First, hindsight's function in germ-band retraction may be limited to maintenance of the amnioserosa which then plays a physical role in the retraction process through contact with cells of the epidermal ectoderm. Second, hindsight might function both to maintain the amnioserosa and to regulate chemical signaling from the amnioserosa to the epidermal ectoderm, thus coordinating the cell shape changes and movements that drive germ-band retraction.

Regulatory network for cell shape changes during Drosophila ventral furrow formation

2006 ◽  
Vol 239 (1) ◽  
pp. 49-62 ◽  
Author(s):  
Julio Aracena ◽  
Mauricio González ◽  
Alejandro Zuñiga ◽  
Marco A. Mendez ◽  
Verónica Cambiazo
Keyword(s):  
Regulatory Network ◽  
Cell Shape ◽  
Ventral Furrow ◽  
Cell Shape Changes ◽  
Shape Changes

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.

scholarly journals Combinatorial patterns of graded RhoA activation and uniform F-actin depletion promote tissue curvature

2020 ◽  
Author(s):  
Marlis Denk-Lobnig ◽  
Natalie C Heer ◽  
Adam C Martin
Keyword(s):  
Gene Expression ◽  
Cell Mechanics ◽  
Cell Shape ◽  
Quantitative Imaging ◽  
Expression Patterns ◽  
Rhoa Activation ◽  
Ventral Furrow ◽  
Distinct Cell ◽  
Cell Shape Changes ◽  
Shape Changes

AbstractDuring development, gene expression regulates cell mechanics and shape to sculpt tissues. Epithelial folding proceeds through distinct cell shape changes that occur in different regions of a tissue. Here, using quantitative imaging in Drosophila melanogaster, we investigate how patterned cell shape changes promote tissue bending during early embryogenesis. We find that the transcription factors Twist and Snail combinatorially regulate a unique multicellular pattern of junctional F-actin density, which corresponds to whether cells apically constrict, stretch, or maintain their shape. Part of this pattern is a gradient in junctional F-actin and apical myosin-2, and the width of this gradient regulates tissue curvature. The actomyosin gradient results from a gradient in RhoA activation that is refined by a balance between RhoGEF2 and the RhoGAP C-GAP. Thus, cell behavior in the ventral furrow is choreographed by the interplay of distinct gene expression patterns and this coordination regulates tissue shape.

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.

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