I was in the room when Jennifer gave her talk about the Rosette formation during tissue morphogenesis. Today, I came across another two papers, similarly, using fly embryo to study epithelia compartmentation. All three are nicely done! Very very inspiring ... Although they are all limited to 2D analysis ...
You can do live-cell imaging on it.
Dev Cell. 2006 Oct;11(4):459-70.
Multicellular rosette formation links planar cell polarity to tissue morphogenesis.
Blankenship JT, Backovic ST, Sanny JS, Weitz O, Zallen JA.
Developmental Biology Program, Sloan-Kettering Institute, New York, New York 10021, USA.
Elongation of the body axis is accompanied by the assembly of a polarized cytoarchitecture that provides the basis for directional cell behavior. We find that planar polarity in the Drosophila embryo is established through a sequential enrichment of actin-myosin cables and adherens junction proteins in complementary surface domains. F-actin accumulation at AP interfaces represents the first break in planar symmetry and occurs independently of proper junctional protein distribution at DV interfaces. Polarized cells engage in a novel program of locally coordinated behavior to generate multicellular rosette structures that form and resolve in a directional fashion. Actin-myosin structures align across multiple cells during rosette formation, and adherens junction proteins assemble in a stepwise fashion during rosette resolution. Patterning genes essential for axis elongation selectively affect the frequency and directionality of rosette formation. We propose that the generation of higher-order rosette structures links local cell interactions to global tissue reorganization during morphogenesis.
You can do chromophore-assisted laser inactivation (CALI) on it!
Nat Cell Biol. 2010 Jan;12(1):60-5; sup pp 1-9. Epub 2009 Dec 6.
An actomyosin-based barrier inhibits cell mixing at compartmental boundaries in Drosophila embryos.
Monier B, Pélissier-Monier A, Brand AH, Sanson B.
Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK. firstname.lastname@example.org
Partitioning tissues into compartments that do not intermix is essential for the correct morphogenesis of animal embryos and organs. Several hypotheses have been proposed to explain compartmental cell sorting, mainly differential adhesion, but also regulation of the cytoskeleton or of cell proliferation. Nevertheless, the molecular and cellular mechanisms that keep cells apart at boundaries remain unclear. Here we demonstrate, in early Drosophila melanogaster embryos, that actomyosin-based barriers stop cells from invading neighbouring compartments. Our analysis shows that cells can transiently invade neighbouring compartments, especially when they divide, but are then pushed back into their compartment of origin. Actomyosin cytoskeletal components are enriched at compartmental boundaries, forming cable-like structures when the epidermis is mitotically active. When MyoII (non-muscle myosin II) function is inhibited, including locally at the cable by chromophore-assisted laser inactivation (CALI), in live embryos, dividing cells are no longer pushed back, leading to compartmental cell mixing. We propose that local regulation of actomyosin contractibility, rather than differential adhesion, is the primary mechanism sorting cells at compartmental boundaries.
You can even use it to test the model!
Curr Biol. 2009 Dec 1;19(22):1950-5. Epub 2009 Oct 29.
Increased cell bond tension governs cell sorting at the Drosophila anteroposterior compartment boundary.
Landsberg KP, Farhadifar R, Ranft J, Umetsu D, Widmann TJ, Bittig T, Said A, Jülicher F, Dahmann C.
Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Subdividing proliferating tissues into compartments is an evolutionarily conserved strategy of animal development [1-6]. Signals across boundaries between compartments can result in local expression of secreted proteins organizing growth and patterning of tissues [1-6]. Sharp and straight interfaces between compartments are crucial for stabilizing the position of such organizers and therefore for precise implementation of body plans. Maintaining boundaries in proliferating tissues requires mechanisms to counteract cell rearrangements caused by cell division; however, the nature of such mechanisms remains unclear. Here we quantitatively analyzed cell morphology and the response to the laser ablation of cell bonds in the vicinity of the anteroposterior compartment boundary in developing Drosophila wings. We found that mechanical tension is approximately 2.5-fold increased on cell bonds along this compartment boundary as compared to the remaining tissue. Cell bond tension is decreased in the presence of Y-27632 , an inhibitor of Rho-kinase whose main effector is Myosin II . Simulations using a vertex model  demonstrate that a 2.5-fold increase in local cell bond tension suffices to guide the rearrangement of cells after cell division to maintain compartment boundaries. Our results provide a physical mechanism in which the local increase in Myosin II-dependent cell bond tension directs cell sorting at compartment boundaries.
There is an obvious trend in cell biology: single cellular events to multi-cellular group activities. What do you think?
New in 'Theory'
- A clustering-outgrowth model for filopodia formation, based on study using Xenopus egg extracts and liposome
- Xenogeneic organ complementation is achievable! What's next? Human-pig chimera?
- Septins, planar cell polarity, cilia, convergent extension ... Bardet-Biedl and Meckel-Gruber syndromes
- Early-passage iPSCs retain cell-of-origin epigenetic memory, which needs continuous passaging to get into Limbo
- Right place and right time: small molecules reprogram cell fate of worm germ cells
- Caspase cleavage-mediated substrate change: switching function of Dicer between RNAi pathway and apoptosis pathway
- Some thoughts on focal adhesion disassembly: focal adhesion fades as retrograde flow