Formation of the notochord in living ascidian embryos

Development ◽  
1985 ◽  
Vol 86 (1) ◽  
pp. 1-17
Author(s):  
David M. Miyamoto

The dynamic behaviour of cells during formation of the notochord in the ascidian, Ciona intestinalis, was examined by means of Differential Interference Contrast (DIC) microscopy and time-lapse videorecording. The initial rudiment is formed in part as a consequence of the pattern of mitotic divisions as the blastopore shifts posteriorly. Vertical and horizontal rearrangements produce an elongate rod of disc-shaped cells stacked end to end. Further elongation is accompanied by a cell shape change. Some cell growth or swelling is indicated to occur later in development, but this growth appears to contribute mostly to an increase in the diameter, and only insignificantly to the length of the notochord. Intracellular vacuoles that appear around 13 h after fertilization increase in size and fuse at about 16 h to form intercellular ones. These in turn merge to form the central matrix core of the notochord at around 18 to 20 h. As the notochord elongates and cells change in shape, the basal surfaces bleb actively. This surface activity may be related to formation of the perinotochordal sheath.

Science ◽  
2012 ◽  
Vol 335 (6073) ◽  
pp. 1232-1235 ◽  
Author(s):  
Minna Roh-Johnson ◽  
Gidi Shemer ◽  
Christopher D. Higgins ◽  
Joseph H. McClellan ◽  
Adam D. Werts ◽  
...  

2014 ◽  
Vol 206 (3) ◽  
pp. 435-450 ◽  
Author(s):  
Claudia G. Vasquez ◽  
Mike Tworoger ◽  
Adam C. Martin

Apical constriction is a cell shape change that promotes epithelial bending. Activation of nonmuscle myosin II (Myo-II) by kinases such as Rho-associated kinase (Rok) is important to generate contractile force during apical constriction. Cycles of Myo-II assembly and disassembly, or pulses, are associated with apical constriction during Drosophila melanogaster gastrulation. It is not understood whether Myo-II phosphoregulation organizes contractile pulses or whether pulses are important for tissue morphogenesis. Here, we show that Myo-II pulses are associated with pulses of apical Rok. Mutants that mimic Myo-II light chain phosphorylation or depletion of myosin phosphatase inhibit Myo-II contractile pulses, disrupting both actomyosin coalescence into apical foci and cycles of Myo-II assembly/disassembly. Thus, coupling dynamic Myo-II phosphorylation to upstream signals organizes contractile Myo-II pulses in both space and time. Mutants that mimic Myo-II phosphorylation undergo continuous, rather than incremental, apical constriction. These mutants fail to maintain intercellular actomyosin network connections during tissue invagination, suggesting that Myo-II pulses are required for tissue integrity during morphogenesis.


2014 ◽  
Vol 54 (4) ◽  
pp. 221-225
Author(s):  
Hiromi MIYOSHI ◽  
Taiji ADACHI

2010 ◽  
Vol 341 (1) ◽  
pp. 5-19 ◽  
Author(s):  
Jacob M. Sawyer ◽  
Jessica R. Harrell ◽  
Gidi Shemer ◽  
Jessica Sullivan-Brown ◽  
Minna Roh-Johnson ◽  
...  

Development ◽  
1987 ◽  
Vol 101 (4) ◽  
pp. 659-671 ◽  
Author(s):  
R.A. McCarthy ◽  
M.M. Burger

Laminin, a component of the embryonic sea urchin basal lamina, is recognized by monoclonal antibody BL1 (Mab BL1). Our results demonstrate that laminin is secreted into the blastcoel at the early blastula stage at a time when the blastomeres undergo a cell shape change and are organized into an epithelium. Laminin is present on the basal surfaces of ectodermal cells and is absent or reduced on migrating primary mesenchyme cells. Microinjection of a monoclonal antibody directed against laminin induces a morphological change in cell shape and a deformation of the embryonic epithelium. Investigation of selected stages of live embryos suggests that the distribution of laminin may be heterogeneous within the basal lamina during early development. The results implicate laminin as a mediator of cell shape change during early morphogenesis.


Development ◽  
2002 ◽  
Vol 129 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Edwin M. Munro ◽  
Garrett Odell

The ascidian notochord forms through simultaneous invagination and convergent extension of a monolayer epithelial plate. Here we combine micromanipulation with time lapse and confocal microscopy to examine how notochord-intrinsic morphogenetic behaviors and interactions with surrounding tissues, determine these global patterns of movement. We show that notochord rudiments isolated at the 64-cell stage divide and become motile with normal timing; but, in the absence of interactions with non-notochordal tissues, they neither invaginate nor converge and extend. We find that notochord formation is robust in the sense that no particular neighboring tissue is required for notochord formation. Basal contact with either neural plate or anterior endoderm/lateral mesenchyme or posterior mesoderm are each alone sufficient to ensure that the notochord plate forms and extends a cylindrical rod. Surprisingly, the axis of convergent extension depends on the specific tissues that contact the notochord, as do other patterns of cell shape change, movement and tissue deformation that accompany notochord formation. We characterize one case in detail, namely, embryos lacking neural plates, in which a normal notochord forms but by an entirely different trajectory. Our results show ascidian notochord formation to be regulative in a fashion and to a degree never before appreciated. They suggest this regulative behavior depends on a complex interplay between morphogenetic tendencies intrinsic to the notochord plate and instructive and permissive interactions with surrounding tissues. We discuss mechanisms that could account for these data and what they imply about notochord morphogenesis and its evolution within the chordate phylum.


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