scholarly journals The first “Slit” is the deepest: the secret to a hollow heart

2008 ◽  
Vol 182 (2) ◽  
pp. 221-223 ◽  
Author(s):  
Iiro Taneli Helenius ◽  
Greg J. Beitel
Keyword(s):  
Cell Shape ◽  
Vascular System ◽  
Hollow Heart ◽  
Autocrine Signaling ◽  
Lumen Formation ◽  
Membrane Surfaces ◽  
Vascular Morphogenesis ◽  
Cell Biol ◽  
Shape Changes

Tubular organs are essential for life, but lumen formation in nonepithelial tissues such as the vascular system or heart is poorly understood. Two studies in this issue (Medioni, C., M. Astier, M. Zmojdzian, K. Jagla, and M. Sémériva. 2008. J. Cell Biol. 182:249–261; Santiago-Martínez, E., N.H. Soplop, R. Patel, and S.G. Kramer. 2008. J. Cell Biol. 182:241–248) reveal unexpected roles for the Slit–Robo signaling system during Drosophila melanogaster heart morphogenesis. In cardioblasts, Slit and Robo modulate the cell shape changes and domains of E-cadherin–based adhesion that drive lumen formation. Furthermore, in contrast to the well-known paracrine role of Slit and Robo in guiding cell migrations, here Slit and Robo may act by autocrine signaling. In addition, the two groups demonstrate that heart lumen formation is even more distinct from typical epithelial tubulogenesis mechanisms because the heart lumen is bounded by membrane surfaces that have basal rather than apical attributes. As the D. melanogaster cardioblasts are thought to have significant evolutionary similarity to vertebrate endothelial and cardiac lineages, these findings are likely to provide insights into mechanisms of vertebrate heart and vascular morphogenesis.

scholarly journals Cells in tight spaces: the role of cell shape in cell function

2010 ◽  
Vol 191 (2) ◽  
pp. 233-236 ◽  
Author(s):  
Jagesh V. Shah
Keyword(s):  
Primary Cilium ◽  
Cell Shape ◽  
Cell Function ◽  
Cellular Function ◽  
Cell Geometry ◽  
Intracellular Organization ◽  
Cell Biol

In this issue, Pitaval et al. (2010. J. Cell Biol. doi:10.1083/jcb.201004003) demonstrate that cell geometry can regulate the elaboration of a primary cilium. Their findings and approaches are part of a historical line of inquiry investigating the role of cell shape in intracellular organization and cellular function.

scholarly journals Using Bcr-Abl to Examine Mechanisms by Which Abl Kinase Regulates Morphogenesis in Drosophila

2008 ◽  
Vol 19 (1) ◽  
pp. 378-393 ◽  
Author(s):  
Traci L. Stevens ◽  
Edward M. Rogers ◽  
Laura M. Koontz ◽  
Donald T. Fox ◽  
Catarina C.F. Homem ◽  
...  
Keyword(s):  
Cell Shape ◽  
Normal Development ◽  
Wild Type ◽  
Nonreceptor Tyrosine Kinase ◽  
Abl Kinase ◽  
Embryonic Morphogenesis ◽  
Dose Dependent ◽  
Shape Changes ◽  
Insight Into

Signaling by the nonreceptor tyrosine kinase Abelson (Abl) plays key roles in normal development, whereas its inappropriate activation helps trigger the development of several forms of leukemia. Abl is best known for its roles in axon guidance, but Abl and its relatives also help regulate embryonic morphogenesis in epithelial tissues. Here, we explore the role of regulation of Abl kinase activity during development. We first compare the subcellular localization of Abl protein and of active Abl, by using a phosphospecific antibody, providing a catalog of places where Abl is activated. Next, we explore the consequences for morphogenesis of overexpressing wild-type Abl or expressing the activated form found in leukemia, Bcr-Abl. We find dose-dependent effects of elevating Abl activity on morphogenetic movements such as head involution and dorsal closure, on cell shape changes, on cell protrusive behavior, and on the organization of the actin cytoskeleton. Most of the effects of Abl activation parallel those caused by reduction in function of its target Enabled. Abl activation leads to changes in Enabled phosphorylation and localization, suggesting a mechanism of action. These data provide new insight into how regulated Abl activity helps direct normal development and into possible biological functions of Bcr-Abl.

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 Cytoskeleton Dynamics in Peripheral T Cell Lymphomas: An Intricate Network Sustaining Lymphomagenesis

2021 ◽  
Vol 11 ◽  
Author(s):  
Valentina Fragliasso ◽  
Annalisa Tameni ◽  
Giorgio Inghirami ◽  
Valentina Mularoni ◽  
Alessia Ciarrocchi
Keyword(s):  
T Cell ◽  
Cell Shape ◽  
Aurora Kinase ◽  
T Cell Lymphomas ◽  
Molecular Landscape ◽  
And Function ◽  
Cytoskeleton Dynamics ◽  
Shape Changes ◽  
Peripheral T Cell Lymphomas

Defects in cytoskeleton functions support tumorigenesis fostering an aberrant proliferation and promoting inappropriate migratory and invasive features. The link between cytoskeleton and tumor features has been extensively investigated in solid tumors. However, the emerging genetic and molecular landscape of peripheral T cell lymphomas (PTCL) has unveiled several alterations targeting structure and function of the cytoskeleton, highlighting its role in cell shape changes and the aberrant cell division of malignant T cells. In this review, we summarize the most recent evidence about the role of cytoskeleton in PTCLs development and progression. We also discuss how aberrant signaling pathways, like JAK/STAT3, NPM-ALK, RhoGTPase, and Aurora Kinase, can contribute to lymphomagenesis by modifying the structure and the signaling properties of cytoskeleton.

50 Hz magnetic fields of varying flux intensity affect cell shape changes in invertebrate immunocytes: The role of potassium ion channels

2002 ◽  
Vol 23 (4) ◽  
pp. 292-297 ◽  
Author(s):  
Enzo Ottaviani ◽  
Davide Malagoli ◽  
Alex Ferrari ◽  
Davide Tagliazucchi ◽  
Angela Conte ◽  
...  
Keyword(s):  
Ion Channels ◽  
Magnetic Fields ◽  
Cell Shape ◽  
Potassium Ion ◽  
Potassium Ion Channels ◽  
Flux Intensity ◽  
Cell Shape Changes ◽  
Shape Changes

scholarly journals Endothelial cells on the move: dynamics in vascular morphogenesis and disease

2020 ◽  
Vol 2 (1) ◽  
pp. H29-H43
Author(s):  
Catarina G Fonseca ◽  
Pedro Barbacena ◽  
Claudio A Franco
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Blood Vessels ◽  
Vascular System ◽  
Endothelial Cell Migration ◽  
Network Stability ◽  
Cell Dynamics ◽  
Vascular Morphogenesis ◽  
Endothelial Cell Differentiation ◽  
Shape Changes

The vascular system is a hierarchically organized network of blood vessels that play crucial roles in embryogenesis, homeostasis and disease. Blood vessels are built by endothelial cells – the cells lining the interior of blood vessels – through a process named vascular morphogenesis. Endothelial cells react to different biomechanical signals in their environment by adjusting their behavior to: (1) invade, proliferate and fuse to form new vessels (angiogenesis); (2) remodel, regress and establish a hierarchy in the network (patterning); and (3) maintain network stability (quiescence). Each step involves the coordination of endothelial cell differentiation, proliferation, polarity, migration, rearrangements and shape changes to ensure network integrity and an efficient barrier between blood and tissues. In this review, we highlighted the relevance and the mechanisms involving endothelial cell migration during different steps of vascular morphogenesis. We further present evidence on how impaired endothelial cell dynamics can contribute to pathology.

scholarly journals Transcriptional regulation of cell shape during organ morphogenesis

2018 ◽  
Vol 217 (9) ◽  
pp. 2987-3005 ◽  
Author(s):  
Aravind Sivakumar ◽  
Natasza A. Kurpios
Keyword(s):  
Transcriptional Regulation ◽  
Cell Shape ◽  
Evolutionary Conservation ◽  
Model Organisms ◽  
Critical Question ◽  
Organ Morphogenesis ◽  
Open Questions ◽  
Cell Shape Changes ◽  
Shape Changes

The emerging field of transcriptional regulation of cell shape changes aims to address the critical question of how gene expression programs produce a change in cell shape. Together with cell growth, division, and death, changes in cell shape are essential for organ morphogenesis. Whereas most studies of cell shape focus on posttranslational events involved in protein organization and distribution, cell shape changes can be genetically programmed. This review highlights the essential role of transcriptional regulation of cell shape during morphogenesis of the heart, lungs, gastrointestinal tract, and kidneys. We emphasize the evolutionary conservation of these processes across different model organisms and discuss perspectives on open questions and research avenues that may provide mechanistic insights toward understanding birth defects.

Actomyosin contraction of the posterior hemisphere is required for inversion of the Volvox embryo

Development ◽  
1999 ◽  
Vol 126 (10) ◽  
pp. 2117-2127
Author(s):  
I. Nishii ◽  
S. Ogihara
Keyword(s):  
Cell Shape ◽  
Posterior Pole ◽  
Principal Role ◽  
Equatorial Diameter ◽  
Pass Through ◽  
Actomyosin Contraction ◽  
Inside Out ◽  
Shape Changes ◽  
Complete Inversion

During inversion of a Volvox embryo, a series of cell shape changes causes the multicellular sheet to bend outward, and propagation of the bend from the anterior to the posterior pole eventually results in an inside-out spherical sheet of cells. We use fluorescent and electron microscopy to study the behavior of the cytoskeleton in cells undergoing shape changes. Microtubules are aligned parallel to the cell's long axis and become elongated in the bend. Myosin and actin filaments are arrayed perinuclearly before inversion. In inversion, actin and myosin are located in a subnuclear position throughout the uninverted region but this localization is gradually lost towards the bend. Actomyosin inhibitors cause enlargement of the embryo. The bend propagation is inhibited halfway and, as a consequence, the posterior hemisphere remains uninverted. The arrested posterior hemisphere will resume and complete inversion even in the presence of an actomyosin inhibitor if the anterior hemisphere is removed microsurgically. We conclude that the principal role of actomyosin in inversion is to cause a compaction of the posterior hemisphere; unless the equatorial diameter of the embryo is reduced in this manner, it is too large to pass through the opening defined by the already-inverted anterior hemisphere.

scholarly journals Pulsed actomyosin contractions in morphogenesis

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 142 ◽  
Author(s):  
Ann Sutherland ◽  
Alyssa Lesko
Keyword(s):  
Cell Shape ◽  
Normal Development ◽  
Tissue Growth ◽  
Model Systems ◽  
Cellular Processes ◽  
Cytoskeletal Networks ◽  
And Migration ◽  
Shape Changes

Cell and tissue shape changes are the fundamental elements of morphogenesis that drive normal development of embryos into fully functional organisms. This requires a variety of cellular processes including establishment and maintenance of polarity, tissue growth and apoptosis, and cell differentiation, rearrangement, and migration. It is widely appreciated that the cytoskeletal networks play an important role in regulating many of these processes and, in particular, that pulsed actomyosin contractions are a core cellular mechanism driving cell shape changes and cell rearrangement. In this review, we discuss the role of pulsed actomyosin contractions during developmental morphogenesis, advances in our understanding of the mechanisms regulating actomyosin pulsing, and novel techniques to probe the role of pulsed actomyosin processes in in vivo model systems.

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