Vaughan KT.TIP maker and TIP marker; EB1 as a master controller of microtubule plus ends. J Cell Biol 171:197-200

Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46556, USA.
The Journal of Cell Biology (Impact Factor: 9.83). 11/2005; 171(2):197-200. DOI: 10.1083/jcb.200509150
Source: PubMed


The EB1 protein is a member of the exciting and enigmatic family of microtubule (MT) tip-tracking proteins. EB1 acts as an exquisite marker of dynamic MT plus ends in some cases, whereas in others EB1 is thought to directly dictate the behavior of the plus ends. How EB1 differentiates between these two roles remains unclear; however, a growing list of interactions between EB1 and other MT binding proteins suggests there may be a single mechanism. Adding another layer of complexity to these interactions, two studies published in this issue implicate EB1 in cross-talk between mitotic MTs and between MTs and actin filaments (Goshima et al., p. 229; Wu et al., p. 201). These results raise the possibility that EB1 is a central player in MT-based transport, and that the activity of MT-binding proteins depends on their ability or inability to interact with EB1.

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Available from: Kevin Vaughan, Jun 22, 2015
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    • "Capture sites often contain actin and EB1 is known to mediate interactions between microtubules and actin in some cell types (reviewed in ref.[113]). The interactions of microtubule ends with capture sites serves several functions including the targeted delivery of vesicles, signaling molecules, and ion channels to specific places in the cell[113,114,122123124125126127128129130131. Whether a similar system operates in plant cells is not known. "

    Full-text · Dataset · Jan 2016
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    • "Functionality of microtubule plus ends can be modified by a set of specialised proteins termed +TIPs that are able to stably associate with the growing end (Akhmanova and Steinmetz, 2008; Perez et al., 1999). Among +TIPs, the members of the EB1 and CLIP-170 families play a central role: EB1 proteins are required for the plus end tracking of other proteins (Akhmanova and Steinmetz, 2008; Honnappa et al., 2009; Vaughan, 2005), while members of the CLIP-170 family are positive regulators of MT growth (Brunner and Nurse, 2000; Komarova et al., 2002; Steinmetz and Akhmanova, 2008). Yeast homologues of EB1 (Bim1) and CLIP170 (Bik1) are both involved in spindle positioning during mitosis of S. cerevisiae. "
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    ABSTRACT: The S. cerevisiae kinesin Kip2 stabilises astral microtubules and facilitates spindle positioning through transport of microtubule-associated proteins, such as the yeast CLIP-170 homologue Bik1, dynein and the Adenomatous Polyposis Coli-related protein Kar9 to the plus ends of astral microtubules.Here, we show that Kip2 associates physically with its processivity factor Bim1, the yeast homologue of the EB1 plus end-tracking protein. This interaction requires an EB1-binding motif in the N-terminal extension of Kip2 and is negatively regulated by phosphorylation through Mck1, the yeast Glycogen Synthase Kinase 3. In addition, Mck1-dependent phosphorylation decreases the intrinsic microtubule affinity of Kip2. Reduction in Kip2 phosphorylation leads to stabilisation of astral microtubules and accumulation of Kip2, dynein and Kar9 at microtubule plus ends, while loss of Mck1 function leads to defects in spindle positioning. Furthermore, we provide evidence that a subpopulation of Mck1 at the bud-cortex phosphorylates Kip2. We propose that yeast GSK-3 spatially controls astral microtubule dynamics and the loading of dynein and Kar9 on astral microtubule plus ends by regulating Kip2 interactions with Bim1 and microtubules.
    Full-text · Article · Sep 2015 · Journal of Cell Science
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    • "Dynamics of microtubule plus ends is reduced in shade Dynamics of microtubule plus ends can be tracked using plus end-binding protein, EB1 (Chan et al. 2003; Vaughan 2005). We used 35Spro::EB1b-GFP transgenic line to study how shade influences the dynamics of cMT plus ends. "
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    ABSTRACT: When sun plants, such as Arabidopsis thaliana, are under canopy shade, elongation of stems/petioles will be induced as one of the most prominent responses. Plant hormones mediate the elongation growth. However, how environmental and hormonal signals are translated into cell expansion activity that leads to the elongation growth remains elusive. Through forward genetic study, we identified \shade avoidance2 (sav2) mutant, which contains a P287L mutation in β-TUBULIN 4. Cortical microtubules (cMTs) play a key role in anisotropic cell growth. Hypocotyls of sav2 are wild type-like in white light, but are short and highly swollen in shade and dark. We showed that shade not only induces cMT rearrangement, but also affects cMT stability and dynamics of plus ends. Even though auxin and brassinosteroids are required for shade-induced hypocotyl elongation, they had little effect on shade-induced rearrangement of cMTs. Blocking auxin transport suppressed dark phenotypes of sav2, while over-expressing EB1b-GFP, a microtubule plus-end binding protein, rescued sav2 in both shade and dark, suggesting that tub4(P287L) represents a unique type of tubulin mutation that does not affect cMT function in supporting cell elongation, but may affect the ability of cMTs to respond properly to growth promoting stimuli. This article is protected by copyright. All rights reserved.
    Full-text · Article · Apr 2015 · Journal of Integrative Plant Biology
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