scholarly journals Chris Bakal: Look and learn

2013 ◽  
Vol 203 (3) ◽  
pp. 378-379
Author(s):  
Caitlin Sedwick
Keyword(s):  
Cell Shape ◽  
Control Cell ◽  
Signaling Networks

Bakal studies the signaling networks that control cell shape.

EB1 Is Essential for Spindle Formation and Chromosome Alignment During Oocyte Meiotic Maturation in Mice

2021 ◽  
pp. 1-7
Author(s):  
Dongjie Zhou ◽  
Zheng-Wen Nie ◽  
Xiang-Shun Cui
Keyword(s):  
Cell Shape ◽  
Control Cell ◽  
Meiotic Maturation ◽  
Junctional Complex ◽  
Spindle Formation ◽  
Oocyte Meiosis ◽  
Polarized Cell Growth ◽  
Chromosome Alignment ◽  
Oocyte Meiotic Maturation

The cytoskeleton plays an orchestrating role in polarized cell growth. Microtubules (MTs) not only play critical roles in chromosome alignment and segregation but also control cell shape, division, and motility. A member of the plus-end tracking proteins, end-binding protein 1 (EB1), regulates MT dynamics and plays vital roles in maintaining spindle symmetry and chromosome alignment during mitosis. However, the role of EB1 in mouse oocyte meiosis remains unknown. Here, we examined the localization patterns and expression levels of EB1 at different stages. EB1 protein level was found to be stable during meiosis. EB1 mainly localized along the spindle and had a similar localization pattern as that of α-tubulin. The EB1 protein was degraded with a Trim-Away method, and the results were further confirmed with western blotting and immunofluorescence. At 12 h of culture after EB1 knockdown (KD), a reduced number of mature MII oocytes were observed. EB1 KD led to spindle disorganization, chromosome misalignment, and missegregation; β-catenin protein binds to actin via the adherens junctional complex, which was significantly reduced in the EB1 KD oocytes. Collectively, we propose that the impairment of EB1 function manipulates spindle formation, thereby promoting chromosomal loss, which is expected to fuel aneuploidy and possibly fertilization failure.

scholarly journals Shape and volume changes in erythrocyte ghosts and spectrin-actin networks.

1980 ◽  
Vol 86 (2) ◽  
pp. 371-376 ◽  
Author(s):  
R M Johnson ◽  
G Taylor ◽  
D B Meyer
Keyword(s):  
Erythrocyte Membrane ◽  
Cell Shape ◽  
Electrolyte Concentration ◽  
Control Cell ◽  
Erythrocyte Ghosts ◽  
Volume Changes ◽  
Sulfhydryl Reagents ◽  
Actin Networks ◽  
Energy Dependent ◽  
Shape Changes

In response to changes in electrolyte concentration and pH, erythrocyte ghosts can exhibit some of the characteristic shapes seen in the intact erythrocyte. These shape changes are accompanied by volume changes; both are reversible, not energy dependent, and not inhibited by sulfhydryl reagents. The volume reduction can also be seen in isolated Triton-free spectrin-actin lattices, showing that this network is capable of reversible contraction. The results suggest that reversible changes in size of the underlying cytoskeleton of the erythrocyte membrane can control cell shape.

scholarly journals Two independent spiral structures control cell shape in Caulobacter

2005 ◽  
Vol 102 (51) ◽  
pp. 18608-18613 ◽  
Author(s):  
N. A. Dye ◽  
Z. Pincus ◽  
J. A. Theriot ◽  
L. Shapiro ◽  
Z. Gitai
Keyword(s):  
Cell Shape ◽  
Control Cell ◽  
Spiral Structures

Optimizing micropattern geometries for cell shape and migration with genetic algorithms

2016 ◽  
Vol 8 (7) ◽  
pp. 741-750 ◽  
Author(s):  
Philipp J. Albert ◽  
Ulrich S. Schwarz
Keyword(s):  
Cell Culture ◽  
Genetic Algorithms ◽  
Cell Shape ◽  
Control Cell ◽  
Standard Tool ◽  
And Migration ◽  
And Function

Adhesive micropatterns have become a standard tool to control cell shape and function in cell culture.

scholarly journals Passive Mechanical Forces Control Cell-Shape Change during Drosophila Ventral Furrow Formation

2014 ◽  
Vol 107 (4) ◽  
pp. 998-1010 ◽  
Author(s):  
Oleg Polyakov ◽  
Bing He ◽  
Michael Swan ◽  
Joshua W. Shaevitz ◽  
Matthias Kaschube ◽  
...  
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Control Cell ◽  
Mechanical Forces ◽  
Cell Shape Change ◽  
Ventral Furrow

scholarly journals Integration of contractile forces during tissue invagination

2010 ◽  
Vol 188 (5) ◽  
pp. 735-749 ◽  
Author(s):  
Adam C. Martin ◽  
Michael Gelbart ◽  
Rodrigo Fernandez-Gonzalez ◽  
Matthias Kaschube ◽  
Eric F. Wieschaus
Keyword(s):  
Cell Shape ◽  
Control Cell ◽  
Adherens Junction ◽  
Tissue Level ◽  
Epithelial Morphogenesis ◽  
Apical Constriction ◽  
Contractile Forces ◽  
Actomyosin Cytoskeleton ◽  
Cellular Forces ◽  
Anterior Posterior

Contractile forces generated by the actomyosin cytoskeleton within individual cells collectively generate tissue-level force during epithelial morphogenesis. During Drosophila mesoderm invagination, pulsed actomyosin meshwork contractions and a ratchet-like stabilization of cell shape drive apical constriction. Here, we investigate how contractile forces are integrated across the tissue. Reducing adherens junction (AJ) levels or ablating actomyosin meshworks causes tissue-wide epithelial tears, which release tension that is predominantly oriented along the anterior–posterior (a-p) embryonic axis. Epithelial tears allow cells normally elongated along the a-p axis to constrict isotropically, which suggests that apical constriction generates anisotropic epithelial tension that feeds back to control cell shape. Epithelial tension requires the transcription factor Twist, which stabilizes apical myosin II, promoting the formation of a supracellular actomyosin meshwork in which radial actomyosin fibers are joined end-to-end at spot AJs. Thus, pulsed actomyosin contractions require a supracellular, tensile meshwork to transmit cellular forces to the tissue level during morphogenesis.

scholarly journals RhoGAP RGA-8 supports morphogenesis in C. elegans by polarizing epithelia through CDC-42

2019 ◽  
Author(s):  
Hamidah Raduwan ◽  
Shashikala Sasidharan ◽  
Luigy Cordova Burgos ◽  
Andre G. Wallace ◽  
Martha C. Soto
Keyword(s):  
Cell Shape ◽  
Control Cell ◽  
Molecular Data ◽  
Regulatory Motifs ◽  
C Elegans ◽  
Cell Embryo ◽  
Embryonic Morphogenesis ◽  
The One ◽  
Muscle Myosin ◽  
Shape Changes

AbstractCDC-42 regulation of non-muscle myosin/NMY-2 is required for polarity maintenance in the one-cell embryo of C. elegans. CDC-42 and NMY-2 regulate polarity throughout embryogenesis, but their contribution to later events of morphogenesis are less understood. We have shown that epidermal enclosure requires the GTPase CED-10/Rac1 and WAVE/Scar complex, its effector, to promote protrusions that drive enclosure through the branch actin regulator Arp2/3. Our analysis here of RGA-8, a homolog of SH3BP1/Rich1/ARHGAP17/Nadrin, with BAR and RhoGAP motifs, suggests it regulates CDC-42, so that NMY-2 promotes two events of epidermal morphogenesis: ventral enclosure and elongation. Genetic and molecular data suggest RGA-8 regulates CDC-42, and the CDC-42 effectors WSP-1 and MRCK-1, in parallel to F-BAR proteins TOCA-1 and TOCA-2. The RGA-8-CDC-42-WSP-1 pathway enriches myosin in migrating epidermal cells during ventral enclosure. We propose TOCA proteins and RGA-8 use BAR domains to localize and regenerate CDC-42 activity, thus regulating F-actin levels, through the branched actin regulator WSP-1, and myosin polarity through the myosin kinase MRCK-1. Regulated CDC-42 thus polarizes epithelia, to control cell migrations and cell shape changes of embryonic morphogenesis.SummaryRGA-8, a protein with membrane binding and actin regulatory motifs, promotes embryonic morphogenesis by localizing active CDC-42 in developing epithelia, thus controlling actin and actin motors during cell movements.

scholarly journals An inducible AraC that responds to blue light instead of arabinose

2020 ◽  
Author(s):  
Edoardo Romano ◽  
Armin Baumschlager ◽  
Emir Bora Akmeriç ◽  
Navaneethan Palanisamy ◽  
Moustafa Houmani ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Blue Light ◽  
Cell Shape ◽  
Control Cell ◽  
Dna Binding Protein ◽  
Dimerization Domain ◽  
E Coli ◽  
Division Site ◽  
The Many

In Escherichia coli, the operon responsible for the catabolism of L-arabinose is regulated by the dimeric DNA-binding protein AraC. In the absence of L-arabinose, AraC binds to the distal I1 and O2 half-sites, leading to repression of the downstream PBAD promoter. In the presence of the sugar, the dimer changes conformation and binds to the adjacent I1 and I2 half-sites, resulting in the activation of PBAD. Here we engineer blue light-inducible AraC dimers in Escherichia coli (BLADE) by swapping the dimerization domain of AraC with blue light-inducible dimerization domains. Using BLADE to overexpress proteins important for cell shape and division site selection, we reversibly control cell morphology with light. We demonstrate the exquisite light responsiveness of BLADE by employing it to create bacteriographs with an unprecedented quality. We then employ it to perform a medium-throughput characterization of 39 E. coli genes with poorly defined or completely unknown function. Finally, we expand the initial library and create a whole family of BLADE transcription factors (TFs), which we characterize using a novel 96-well light induction setup. Since the PBAD promoter is commonly used by microbiologists, we envisage that the BLADE TFs will bring the many advantages of optogenetic gene expression to the field of microbiology.

scholarly journals Helicobacter pyloriPossesses Four Coiled-Coil-Rich Proteins That Form Extended Filamentous Structures and Control Cell Shape and Motility

2011 ◽  
Vol 193 (17) ◽  
pp. 4523-4530 ◽  
Author(s):  
M. Specht ◽  
S. Schatzle ◽  
P. L. Graumann ◽  
B. Waidner
Keyword(s):  
Cell Shape ◽  
Control Cell ◽  
Coiled Coil ◽  
And Control

scholarly journals FGFR/Heartless and Smog interact synergistically to negatively regulate Fog mediated GPCR signaling

2019 ◽  
Author(s):  
Kumari Shweta ◽  
Anagha Basargekar ◽  
Anuradha Ratnaparkhi
Keyword(s):  
G Protein ◽  
Cell Shape ◽  
Shape Change ◽  
Control Cell ◽  
Negative Regulator ◽  
Fine Tuning ◽  
Dependent Manner ◽  
Gpcr Signaling ◽  
Cell Shape Change ◽  
Embryonic Cns

AbstractG-protein coupled receptor (GPCR) signaling triggered by Folded gastrulation (Fog) is one of the pathways known to regulate glial organization and morphogenesis in the embryonic CNS in Drosophila. Fog is best known for its role in epithelial morphogenesis during gastrulation. Here, the signaling pathway includes GPCRs Mist and Smog and the G-Protein Concertina (Cta) which activate downstream effectors to bring about cytoskeletal changes essential for cell shape changeIn this study, we identify molecular players that mediate and serve as important regulators of Fog signaling in the embryonic CNS. We find that while Cta is essential for Fog signaling neither receptors, Mist nor Smog mediates signaling in the CNS. On the contrary, we find that Smog functions as a negative regulator of the pathway. Surprisingly, Heartless which encodes a fibroblast growth factor receptor, also functions as a negative regulator of Fog signaling. Further, we find that both heartless and smog interact in a synergistic manner to regulate Fog signaling.This study thus identifies novel regulators of Fog signaling that may play an important role in fine-tuning the pathway to control cell morphogenesis. It also suggests the likelihood of there being multiple receptors for Fog that mediate and regulate signaling in a context specific manner.Author SummaryIn Drosophila, Folded gastrulation (Fog) functions as ligand that signals via GPCRs to regulate cell shape during gastrulation -one of the earliest events in embryogenesis. Here, Fog signals via receptors Mist and Smog to activate the G-protein Concertina to elicit change in cell shape. In the embryonic central nervous system (CNS) this pathway regulates shape and organization of glia important for functions such as insulation of neurons and synapses.The mechanism of Fog signal transduction in the CNS and its regulation is not well understood. We have sought to address these questions in our study. We find that Concertina is an essential factor for Fog signaling in the CNS but interestingly Mist is not. In contrast, Smog functions as a negative regulator such that loss of Smog enhances Fog signaling. A similar role is played by the receptor tyrosine kinase-Heartless. Interestingly, we find that Smog and Heartless interact as part of a common genetic network to regulate Fog signaling. Our results thus provide novel insights into the regulation of Fog signaling and shed light on how signaling can be fine-tuned in a context dependent manner to control cell shape change which plays a critical role during development and organ formation.

Sign in / Sign up

Export Citation Format

Share Document