scholarly journals 08-P013 Mercury (Drosophila Tubulin Binding Cofactor B) controls cell polarity through the stabilisation of the microtubule network

2009 ◽  
Vol 126 ◽  
pp. S147-S148
Author(s):  
Alexandre Baffet ◽  
Beatrice Benoit ◽  
Vanessa Gourhand ◽  
Claire Heichette ◽  
Denis Chretien ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Microtubule Network ◽  
Tubulin Binding

scholarly journals Drosophila tubulin-binding cofactor B is required for microtubule network formation and for cell polarity

2012 ◽  
Vol 23 (18) ◽  
pp. 3591-3601 ◽  
Author(s):  
Alexandre D. Baffet ◽  
Béatrice Benoit ◽  
Jens Januschke ◽  
Jennifer Audo ◽  
Vanessa Gourhand ◽  
...  
Keyword(s):  
Cell Division ◽  
Cell Polarity ◽  
Intracellular Transport ◽  
Network Formation ◽  
Follicle Cells ◽  
Microtubule Network ◽  
Tubulin Binding ◽  
Associated Proteins ◽  
Dependent Cell

Microtubules (MTs) are essential for cell division, shape, intracellular transport, and polarity. MT stability is regulated by many factors, including MT-associated proteins and proteins controlling the amount of free tubulin heterodimers available for polymerization. Tubulin-binding cofactors are potential key regulators of free tubulin concentration, since they are required for α-β–tubulin dimerization in vitro. In this paper, we show that mutation of the Drosophila tubulin-binding cofactor B (dTBCB) affects the levels of both α- and β-tubulins and dramatically destabilizes the MT network in different fly tissues. However, we find that dTBCB is dispensable for the early MT-dependent steps of oogenesis, including cell division, and that dTBCB is not required for mitosis in several tissues. In striking contrast, the absence of dTBCB during later stages of oogenesis causes major defects in cell polarity. We show that dTBCB is required for the polarized localization of the axis-determining mRNAs within the oocyte and for the apico-basal polarity of the surrounding follicle cells. These results establish a developmental function for the dTBCB gene that is essential for viability and MT-dependent cell polarity, but not cell division.

scholarly journals Tubulin Folding Cofactor TBCB is a Target of the Salmonella Effector Protein SseK1

2020 ◽  
Vol 21 (9) ◽  
pp. 3193 ◽  
Author(s):  
Juan Luis Araujo-Garrido ◽  
Fernando Baisón-Olmo ◽  
Joaquín Bernal-Bayard ◽  
Francisco Romero ◽  
Francisco Ramos-Morales
Keyword(s):  
Host Cell ◽  
Type Iii Secretion ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Yeast Two Hybrid ◽  
Microtubule Network ◽  
Binding Partner ◽  
Tubulin Binding ◽  
Serovar Typhimurium ◽  
Novel Target ◽  
Two Hybrid

Salmonella enterica serovar Typhimurium is a human and animal pathogen that uses type III secretion system effectors to manipulate the host cell and fulfill infection. SseK1 is a Salmonella effector with glycosyltransferase activity. We carried out a yeast two-hybrid screen and have identified tubulin-binding cofactor B (TBCB) as a new binding partner for this effector. SseK1 catalyzed the addition of N-acetylglucosamine to arginine on TBCB, and its expression promoted the stabilization of the microtubule cytoskeleton of HEK293T cells. The conserved Asp-x-Asp (DxD) motif that is essential for the activity of SseK1 was required for the binding and modification of TBCB and for the effect on the cytoskeleton. Our study has identified a novel target for SseK1 and suggests that this effector may have a role in the manipulation of the host cell microtubule network to provide a safe niche for this pathogen.

scholarly journals Arl2- and Msps-dependent microtubule growth governs asymmetric division

2016 ◽  
Vol 212 (6) ◽  
pp. 661-676 ◽  
Author(s):  
Keng Chen ◽  
Chwee Tat Koe ◽  
Zhanyuan Benny Xing ◽  
Xiaolin Tian ◽  
Fabrizio Rossi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Cell Polarity ◽  
Control Cell ◽  
Asymmetric Division ◽  
New Paradigm ◽  
Self Renewal ◽  
Tubulin Binding ◽  
Microtubule Growth ◽  
Adp Ribosylation Factor

Asymmetric division of neural stem cells is a fundamental strategy to balance their self-renewal and differentiation. It is long thought that microtubules are not essential for cell polarity in asymmetrically dividing Drosophila melanogaster neuroblasts (NBs; neural stem cells). Here, we show that Drosophila ADP ribosylation factor like-2 (Arl2) and Msps, a known microtubule-binding protein, control cell polarity and spindle orientation of NBs. Upon arl2 RNA intereference, Arl2-GDP expression, or arl2 deletions, microtubule abnormalities and asymmetric division defects were observed. Conversely, overactivation of Arl2 leads to microtubule overgrowth and depletion of NBs. Arl2 regulates microtubule growth and asymmetric division through localizing Msps to the centrosomes in NBs. Moreover, Arl2 regulates dynein function and in turn centrosomal localization of D-TACC and Msps. Arl2 physically associates with tubulin cofactors C, D, and E. Arl2 functions together with tubulin-binding cofactor D to control microtubule growth, Msps localization, and NB self-renewal. Therefore, Arl2- and Msps-dependent microtubule growth is a new paradigm regulating asymmetric division of neural stem cells.

scholarly journals A CLN6-CRMP2-KLC4 complex regulates anterograde ER-derived vesicle trafficking in cortical neurites

2021 ◽  
Author(s):  
Seung Yon Koh ◽  
Jacob T Cain ◽  
Helen Magee ◽  
Katherine A White ◽  
Mitch Rechtzigel ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Batten Disease ◽  
Building Blocks ◽  
Microtubule Network ◽  
Transmembrane Receptors ◽  
Protein Partners ◽  
Complete Restoration ◽  
Tubulin Binding ◽  
The Central Nervous System ◽  
Novel Complex

As neurons establish extensive connections throughout the central nervous system, the transport of cargo along the microtubule network of the axon is crucial for differentiation and homeostasis. Specifically, building blocks such as membrane and cytoskeletal components, organelles, transmembrane receptors, adhesion molecules, and peptide neurotransmitters all require proper transport to the presynaptic compartment. Here, we identify a novel complex regulating vesicular endoplasmic reticulum transport in neurites, composed of CLN6: an ER-associated protein of relatively unknown function implicated in CLN6-Batten disease; CRMP2: a tubulin binding protein important in regulating neurite microtubule dynamics; and KLC4: a classic transport motor protein. We show that this 'CCK' complex allows ER-derived vesicles to migrate to the distal end of the axon, aiding in proper neurite outgrowth and arborization. In the absence of CLN6, the CCK complex does not function effectively, leading to reduced vesicular transport, stunted neurite outgrowth, and deficits in CRMP2 binding to other protein partners. Treatment with a CRMP2 modulating compound, lanthionine ketimine ester, partially restores these deficits in CLN6-deficient mouse neurons, indicating that stabilization of CRMP2 interacting partners may prove beneficial in lieu of complete restoration of the CCK complex. Taken together, these findings reveal a novel mechanism of ER-derived vesicle transport in the axon and provide new insights into therapeutic targets for neurodegenerative disease.

scholarly journals Motor usage imprints microtubule stability in the shaft

2021 ◽  
Author(s):  
Mireia Andreu-Carbo ◽  
Simon Fernandes ◽  
Marie-Claire Celluz ◽  
Karsten Kruse ◽  
Charlotte Aumeier
Keyword(s):  
Motor Activity ◽  
Cell Polarity ◽  
Molecular Motors ◽  
Intracellular Transport ◽  
Average Length ◽  
Microtubule Network ◽  
Microtubule Stability ◽  
Transport Organization

Tubulin dimers assemble into dynamic microtubules which are used by molecular motors as tracks for intracellular transport. Organization and dynamics of the microtubule network is commonly thought to be regulated at the polymer ends, where tubulin-dimers can be added or removed. Here we show that molecular motors running on microtubules cause exchange of dimers along the shaft. These sites of dimer exchange act as rescue sites where depolymerising microtubules stop shrinking and start re-growing. Consequently, the average length of microtubules increases depending on how frequently they are used as motor tracks. An increase of motor activity densifies the cellular microtubule network and enhances cell polarity. Running motors leave marks in the shaft serving as traces of microtubule usage to organize the polarity landscape of the cell.

Theaflavins Depolymerize Microtubule Network through Tubulin Binding and Cause Apoptosis of Cervical Carcinoma HeLa Cells

2011 ◽  
Vol 59 (5) ◽  
pp. 2040-2048 ◽  
Author(s):  
Subhendu Chakrabarty ◽  
Amlan Das ◽  
Abhijit Bhattacharya ◽  
Gopal Chakrabarti
Keyword(s):  
Cervical Carcinoma ◽  
Hela Cells ◽  
Microtubule Network ◽  
Tubulin Binding
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