Specification of cell fates at the dorsal margin of the zebrafish gastrula

Development ◽  
1996 ◽  
Vol 122 (7) ◽  
pp. 2225-2237 ◽  
Author(s):  
A.E. Melby ◽  
R.M. Warga ◽  
C.B. Kimmel
Keyword(s):  
Single Cells ◽  
Homeobox Gene ◽  
Dorsal Margin ◽  
Wild Type ◽  
Fate Map ◽  
Expression Domain ◽  
Kupffer’S Vesicle ◽  
Kupffer's Vesicle ◽  
Mapping Techniques ◽  
Early Gastrula

Using fate mapping techniques, we have analyzed development of cells of the dorsal marginal region in wild-type and mutant zebrafish. We define a domain in the early gastrula that is located just at the margin and centered on the dorsal midline, in which most cells generate clones that develop exclusively as notochord. The borders of the notochord domain are sharp at the level of single cells, and coincide almost exactly with the border of the expression domain of the homeobox gene floating head (flh; zebrafish homologue of Xnot), a gene essential for notochord development. In flh mutants, cells in the notochord domain generate clones of muscle cells. In contrast, notochord domain cells form mesenchyme in embryos mutant for no tail (ntl; zebrafish homologue of Brachyury). A minority of cells in the notochord domain in wild-type embryos develop as unrestricted mesoderm, invariably located in the tail, suggesting that early gastrula expression of flh does not restrict cellular potential to the notochord fate. The unrestricted tail mesodermal fate is also expressed by the forerunner cells, a cluster of cells located outside the blastoderm, adjacent to the notochord domain. We show that cells can leave the dorsal blastoderm to join the forerunners, suggesting that relocation between fate map domains might respecify notochord domain cells to the tail mesodermal fate. An intermediate fate of the forerunners is to form the epithelial lining of Kupffer's vesicle, a transient structure of the teleost tailbud. The forerunners appear to generate the entire structure of Kupffer's vesicle, which also develops in most flh mutants. Although forerunner cells are present in ntl mutants, Kupffer's vesicle never appears, which is correlated with the later severe disruption of tail development.

The ventral and posterior expression of the zebrafish homeobox gene eve1 is perturbed in dorsalized and mutant embryos

Development ◽  
1993 ◽  
Vol 119 (4) ◽  
pp. 1261-1275 ◽  
Author(s):  
J.S. Joly ◽  
C. Joly ◽  
S. Schulte-Merker ◽  
H. Boulekbache ◽  
H. Condamine
Keyword(s):  
Cell Fate ◽  
Zebrafish Embryo ◽  
Marginal Zone ◽  
Posterior Part ◽  
Homeobox Gene ◽  
Migratory Behaviour ◽  
Wild Type ◽  
Tail Region ◽  
Expression Domain ◽  
Tail Tip

We have identified and characterized zebrafish eve1, a novel member of the Drosophila even-skipped (eve) gene family. eve1 RNAs are expressed initially in late blastulae with a peak during the gastrula stage, at which time expression is confined to ventral and lateral cells of the marginal zone of the zebrafish embryo. Later, eve1 transcripts are located in the most posterior part of the extending tail tip. We show that LiCl, known to dorsalize Xenopus embryos, has the same effect in zebrafish, resulting in embryos with exaggerated dorsoanterior structures. In LiCl-treated embryos, eve1 transcripts are completely absent. eve1 is therefore a marker of ventral and posterior cells. In the light of its ventroposterior expression domain, the localization of eve1 transcripts was analysed in spadetail (spt) and no tail (ntl), two mutants with abnormal caudal development. In sptb140 homozygous mutants, there is an accumulation of cells in the tail region, resulting from inadequate migratory behaviour of precursors to the trunk somites. These cells, in their abnormal environment, express eve1, emphasizing the correlation between ventroposterior position and eve1 expression. In homozygous mutant embryos for the gene ntl (the homologue of mouse Brachyury, originally called Zf-T), posterior structures are missing (M. E. Halpern, C. B. Kimmel, R. K. Ho and C. Walker, 1993; Cell In press). While mutant and wild-type embryos do not differ in their eve1 transcript distribution during gastrulation, eve1 expression is absent in the caudal region of mutant ntl embryos during early somitogenesis, indicating a requirement for ntl in the maintenance of eve1 expression during tail extension. Our findings suggest that eve1 expression is correlated with a ventral and posterior cell fate, and provide first insights into its regulation.

scholarly journals Cell volume changes contribute to epithelial morphogenesis in zebrafish Kupffer’s vesicle

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Agnik Dasgupta ◽  
Matthias Merkel ◽  
Madeline J Clark ◽  
Andrew E Jacob ◽  
Jonathan Edward Dawson ◽  
...  
Keyword(s):  
Cell Volume ◽  
Cell Shape ◽  
Single Cells ◽  
Ion Flux ◽  
Epithelial Morphogenesis ◽  
Volume Changes ◽  
Kupffer’S Vesicle ◽  
Kupffer's Vesicle ◽  
Cell Shape Changes ◽  
Shape Changes

How epithelial cell behaviors are coordinately regulated to sculpt tissue architecture is a fundamental question in biology. Kupffer’s vesicle (KV), a transient organ with a fluid-filled lumen, provides a simple system to investigate the interplay between intrinsic cellular mechanisms and external forces during epithelial morphogenesis. Using 3-dimensional (3D) analyses of single cells we identify asymmetric cell volume changes along the anteroposterior axis of KV that coincide with asymmetric cell shape changes. Blocking ion flux prevents these cell volume changes and cell shape changes. Vertex simulations suggest cell shape changes do not depend on lumen expansion. Consistent with this prediction, asymmetric changes in KV cell volume and shape occur normally when KV lumen growth fails due to leaky cell adhesions. These results indicate ion flux mediates cell volume changes that contribute to asymmetric cell shape changes in KV, and that these changes in epithelial morphology are separable from lumen-generated forces.

scholarly journals Asymmetric cell volume changes regulate epithelial morphogenesis in zebrafish Kupffer’s vesicle

2017 ◽  
Author(s):  
Agnik Dasgupta ◽  
Matthias Merkel ◽  
Andrew E. Jacob ◽  
Jonathan Dawson ◽  
M. Lisa Manning ◽  
...  
Keyword(s):  
Cell Volume ◽  
Cell Shape ◽  
Single Cells ◽  
Ion Flux ◽  
Epithelial Morphogenesis ◽  
Volume Changes ◽  
Kupffer’S Vesicle ◽  
Kupffer's Vesicle ◽  
Cell Shape Changes ◽  
Shape Changes

ABSTRACTHow epithelial cell behaviors are coordinately regulated to sculpt tissue architecture is a fundamental question in biology. Kupffer's vesicle (KV), a transient organ with a fluid - filled lumen, provides a simple system to investigate the interplay between intrinsic cellular mechanisms and external forces during epithelial morphogenesis. Using 3 - dimensional (3D) analyses of single cells we identify asymmetric cell volume changes along the anteroposterior axis of KV that coincide with asymmetric cell shape changes. Blocking ion flux prevents these cell volume changes and cell shape changes. Vertex simulations suggest cell shape changes do not depend on lumen expansion. Consistent with this prediction, asymmetric changes in KV cell volume and shape occur normally when KV lumen growth fails due to leaky cell adhesions. These results indicate ion flux mediates asymmetric cell volume changes that contribute to asymmetric cell shape changes in KV, and that these changes in epithelial morphology are separable from lumen - generated forces.

Overexpression of the forebrain-specific homeobox gene six3 induces rostral forebrain enlargement in zebrafish

Development ◽  
1998 ◽  
Vol 125 (15) ◽  
pp. 2973-2982 ◽  
Author(s):  
M. Kobayashi ◽  
R. Toyama ◽  
H. Takeda ◽  
I.B. Dawid ◽  
K. Kawakami
Keyword(s):  
Homeobox Gene ◽  
Cloning And Expression ◽  
Optic Stalk ◽  
Sine Oculis ◽  
Murine Homolog ◽  
Enhanced Expression ◽  
Rostral Region ◽  
The Brain ◽  
Early Gastrula ◽  
Anterior Neural Plate

The Drosophila homeobox gene sine oculis is expressed in the rostral region of the embryo in early development and is essential for eye and brain formation. Its murine homolog, Six3, is expressed in the anterior neural plate and eye anlage, and may have crucial functions in eye and brain development. In this study, we describe the cloning and expression of zebrafish six3, the apparent ortholog of the mouse Six3 gene. Zebrafish six3 transcripts are first seen in hypoblast cells in early gastrula embryos and are found in the anterior axial mesendoderm through gastrulation. six3 expression in the head ectoderm begins at late gastrula. Throughout the segmentation period, six3 is expressed in the rostral region of the prospective forebrain. Overexpression of six3 in zebrafish embryos induced enlargement of the rostral forebrain, enhanced expression of pax2 in the optic stalk and led to a general disorganization of the brain. Disruption of either the Six domain or the homeodomain abolish these effects, implying that these domains are essential for six3 gene function. Our results suggest that the vertebrate Six3 genes are involved in the formation of the rostral forebrain.

Cell-autonomous shift from axial to paraxial mesodermal development in zebrafish floating head mutants

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4257-4264 ◽  
Author(s):  
M.E. Halpern ◽  
C. Thisse ◽  
R.K. Ho ◽  
B. Thisse ◽  
B. Riggleman ◽  
...  
Keyword(s):  
Neural Tube ◽  
Single Cells ◽  
Floor Plate ◽  
Paraxial Mesoderm ◽  
Wild Type ◽  
Genetic Mosaics ◽  
Essential Step ◽  
Ventral Neural Tube ◽  
Mesodermal Development

Zebrafish floating head mutant embryos lack notochord and develop somitic muscle in its place. This may result from incorrect specification of the notochord domain at gastrulation, or from respecification of notochord progenitors to form muscle. In genetic mosaics, floating head acts cell autonomously. Transplanted wild-type cells differentiate into notochord in mutant hosts; however, cells from floating head mutant donors produce muscle rather than notochord in wild-type hosts. Consistent with respecification, markers of axial mesoderm are initially expressed in floating head mutant gastrulas, but expression does not persist. Axial cells also inappropriately express markers of paraxial mesoderm. Thus, single cells in the mutant midline transiently co-express genes that are normally specific to either axial or paraxial mesoderm. Since floating head mutants produce some floor plate in the ventral neural tube, midline mesoderm may also retain early signaling capabilities. Our results suggest that wild-type floating head provides an essential step in maintaining, rather than initiating, development of notochord-forming axial mesoderm.

scholarly journals Bardet–Biedl syndrome genes are important in retrograde intracellular trafficking and Kupffer's vesicle cilia function

2006 ◽  
Vol 15 (5) ◽  
pp. 667-677 ◽  
Author(s):  
Hsan-Jan Yen ◽  
Marwan K. Tayeh ◽  
Robert F. Mullins ◽  
Edwin M. Stone ◽  
Val C. Sheffield ◽  
...  
Keyword(s):  
Intracellular Trafficking ◽  
Bardet Biedl Syndrome ◽  
Kupffer’S Vesicle ◽  
Kupffer's Vesicle

Muscle development is independent of innervation during Drosophila embryogenesis

Development ◽  
1993 ◽  
Vol 119 (2) ◽  
pp. 533-543 ◽  
Author(s):  
K. Broadie ◽  
M. Bate
Keyword(s):  
Time Course ◽  
Muscle Development ◽  
Single Cells ◽  
Drosophila Embryo ◽  
Wild Type ◽  
Type Pattern ◽  
Motor Nerves ◽  
Embryonic Myogenesis ◽  
Peripheral Motor

We have examined the role of innervation in directing embryonic myogenesis, using a mutant (prospero), which delays the pioneering of peripheral motor nerves of the Drosophila embryo. In the absence of motor nerves, myoblasts fuse normally to form syncytial myotubes, myotubes form normal attachments to the epidermis, and a larval musculature comparable to the wild-type pattern is generated and maintained. Likewise, the twist-expressing myoblasts that prefigure the adult musculature segregate normally in the absence of motor nerves, migrate to their final embryonic positions and continue to express twist until the end of embryonic development. In the absence of motor nerves, myotubes uncouple at the correct developmental stage to form single cells. Subsequently, uninnervated myotubes develop the mature electrical and contractile properties of larval muscles with a time course indistinguishable from normally innervated myotubes. We conclude that innervation plays no role in the patterning, morphogenesis, maintenance or physiological development of the somatic muscles in the Drosophila embryo.

Growth in cell length in the fission yeast Schizosaccharomyces pombe

1985 ◽  
Vol 75 (1) ◽  
pp. 357-376 ◽  
Author(s):  
J.M. Mitchison ◽  
P. Nurse
Keyword(s):  
Schizosaccharomyces Pombe ◽  
Cell Size ◽  
Single Cells ◽  
Temperature Shift ◽  
Time Lapse ◽  
Cell Length ◽  
Wild Type ◽  
Cycle Growth ◽  
A Cell ◽  
Mutant Cells

The cylindrical cells of Schizosaccharomyces pombe grow in length by extension at the ends and not the middle. At the beginning of the cell cycle, growth is restricted to the ‘old end’, which existed in the previous cycle. Later on, the ‘new end’, formed from the septum, starts to grow at a point in the cycle that we have called NETO (‘new end take-off’). Fluorescence microscopy on cells stained with Calcofluor has been used to study NETO in size mutants, in blocked cdc mutants and with different growth temperatures and media. In wild-type cells (strain 972) NETO happens at 0.34 of the cycle with a cell length of 9.5 microns. With size mutants that are smaller at division, NETO takes place at the same size (9.0-9.5 microns) but this is not achieved until later in the cycle. Another control operates in larger size mutants since NETO occurs at the same stage of the cycle (about 0.32) as in wild type but at a larger cell size. This control is probably a requirement to have completed an event in early G2, since most cdc mutant cells blocked before this point in the cycle do not show NETO whereas most of those blocked in late G2 do show it. We conclude that NETO only happens if: (1) the cell length is greater than a critical value of 9.0-9.5 microns; and (2) the cell has traversed the first 0.3-0.35 of the cycle and passed early G2. NETO is delayed in poor media, in which cell size is also reduced. Temperature has little effect on NETO under steady-state conditions, but there is a transient delay for some hours after a temperature shift. NETO is later in another wild-type strain, 132. Time-lapse photomicrography was used to follow the rates of length growth in single cells. Wild-type cells showed two linear segments during the first 75% of the cycle. There was a rate-change point (RCP), coincident with NETO, where the rate of total length extension increased by 35%. This increase was not due simply to the start of new-end growth, since old-end growth slowed down in some cells at the RCP. cdc 11.123 is a mutant in which septation and division is blocked at 35 degrees C but nuclear division continues.(ABSTRACT TRUNCATED AT 400 WORDS)

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