Modulation of microtubule shape in vitro by high molecular weight microtubule associated proteins MAP1A, MAP1B, and MAP2

Pedrotti, Barbara; Francolini, Maura; Cotelli, Franco; Islam, Khalid

doi:10.1016/0014-5793(96)00308-0

Cited by 18 publications

(11 citation statements)

References 31 publications

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“…MAP1B is a long, filamentous molecule with a small spherical portion at one end, forming long cross-bridges between microtubules in vitro and in neurons [Sato-Yoshitake et al, 1989] and known to have a strong stabilizing effect on microtubules. Our results demonstrate that both recombinant MAP1B 1404 and MAP1B 981 recovered the ability of MAP1B to promote microtubule assembly, as described previously [Pedrotti and Islam, 1995;Pedrotti et al, 1996], from newborn rat brain MAP1B [Riederer et al, 1986] and from porcine brain MAP1B [Vandecandelaere et al, 1996]. Both fragments contained the MBD, yet the assembly rate was increased nearly by twofold for the larger fragment.…”

Section: Map1b Stabilizing Function On Microtubulessupporting

confidence: 78%

The control of microtubule stability in vitro and in transfected cells by MAP1B and SCG10

Bondallaz

Barbier

Soehrman

et al. 2006

Cell Motil. Cytoskeleton

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In neurons, the regulation of microtubules plays an important role for neurite outgrowth, axonal elongation, and growth cone steering. SCG10 family proteins are the only known neuronal proteins that have a strong destabilizing effect, are highly enriched in growth cones and are thought to play an important role during axonal elongation. MAP1B, a microtubule-stabilizing protein, is found in growth cones as well, therefore it was important to test their effect on microtubules in the presence of both proteins. We used recombinant proteins in microtubule assembly assays and in transfected COS-7 cells to analyze their combined effects in vitro and in living cells, respectively. Individually, both proteins showed their expected activities in microtubule stabilization and destruction respectively. In MAP1B/SCG10 double-transfected cells, MAP1B could not protect microtubules from SCG10-induced disassembly in most cells, in particular not in cells that contained high levels of SCG10. This suggests that SCG10 is more potent to destabilize microtubules than MAP1B to rescue them. In microtubule assembly assays, MAP1B promoted microtubule formation at a ratio of 1 MAP1B per 70 tubulin dimers while a ratio of 1 SCG10 per two tubulin dimers was needed to destroy microtubules. In addition to its known binding to tubulin dimers, SCG10 binds also to purified microtubules in growth cones of dorsal root ganglion neurons in culture. In conclusion, neuronal microtubules are regulated by antagonistic effects of MAP1B and SCG10 and a fine tuning of the balance of these proteins may be critical for the regulation of microtubule dynamics in growth cones.

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Section: Map1b Stabilizing Function On Microtubulessupporting

confidence: 78%

The control of microtubule stability in vitro and in transfected cells by MAP1B and SCG10

Bondallaz

Barbier

Soehrman

et al. 2006

Cell Motil. Cytoskeleton

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“…This protein, which is colocalized with MAP2 on the same microtubules in dendrites (Shiomura and Hirokawa 1987), is much more affected by permanent IM lesion. MAP1A, MAP1B, and MAP2 are thought to modulate not only the microtubule dynamics but also microtubule shape, which may be important for their spatial distribution and/or role in specific neuronal areas (Pedrotti et al 1996). A third MAP, tau, is also known to regulate the organization of the neuronal cytoskeleton (Kwei et al 1998).…”

Section: Discussionmentioning

confidence: 99%

Effects of NaCN and ionomycin on neuronal viability and on the abundance of microtubule-associated proteins MAP1, MAP2, and tau in isolated chick cortical neurons

Hutter‐Paier¹,

Grygar²,

Loibner³

et al. 2000

Cell and Tissue Research

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The effects of two toxins, sodium cyanide (NaCN) and ionomycin (IM), on neuronal viability and on the expression of the microtubule-associated proteins MAP1, MAP2, and tau were studied in isolated chick cortical neurons. Cytotoxic hypoxia due to NaCN treatment was performed to mimic acute neuronal damage, whereas long-term IM treatment was used as a model for chronic neuronal impairment. After 5 days in vitro, a cytotoxic lesion was induced either by addition of NaCN (0.01-10 mM) or IM (0.01-10 microM). The NaCN solution was aspirated after 30 min and cells were allowed to regenerate for 6 h, 24 h, 48 h, or 72 h; whereas the permanent IM lesions were left undisturbed during the same periods of time. Neuronal viability was assessed by MTT assay. The abundance of MAP1, MAP2, and tau was evaluated by immunoblotting and, for MAP2, by immunohistochemistry also. Results showed that NaCN and IM lesions dose-dependently decreased viability. Irreversible cell damage occurred after impairment with 10 mM NaCN and 1 microm or 10 microm IM, while neurons lesioned with lower concentrations regenerated partially or adapted to the toxic environment. However, the same level of viability as of untreated cells was never reached. Furthermore abundance of MAPs was changed after both lesions. But while after extended recovery from NaCN lesion protein expression was normalizing (MAP2) or at least still detectable (MAP1A, tau), the consequences of a permanent IM lesion were more severe, since neurons were not able to maintain or even restore their MAP expression. Immunohistochemical experiments for MAP2 revealed that, compared with controls, NaCN and, to a much higher extent, IM treatment resulted in a loss of immunoreactivity in neurites due to progressing cell death.

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“…Another light chain LC2 (24 kDa) specifically associates with MAP1A. Electron microscopic studies suggested that these protein complexes form long filamentous arms linked to the microtubules and connecting microtubules to each other, and so possibly modulating microtubule shape (Shiomura and Hirokawa, 1987; Sato‐Yoshitake et al ., 1989; Pedrotti et al ., 1996).…”

Section: Discussionmentioning

confidence: 99%

Aut2p and Aut7p, two novel microtubule-associated proteins are essential for delivery of autophagic vesicles to the vacuole

1998

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AUT2 and AUT7, two novel genes essential for autophagocytosis in the yeast Saccharomyces cerevisiae were isolated. AUT7 was identified as a low copy suppressor of autophagic defects in aut2-1 cells. Aut7p is a homologue of the rat microtubule-associated protein (MAP) light chain 3 (LC3). Aut2p and Aut7p interact physically. Aut7p is attached to microtubules via Aut2p, which interacts with tubulins Tub1p and Tub2p. aut2-and aut7-deleted cells are unable to deliver autophagic vesicles and the precursor of aminopeptidase I to the vacuole. Double membrane-layered autophagosome-like vesicles accumulate in the cytoplasm of these cells. Our findings suggest that microtubules and an attached protein complex of Aut2p and Aut7p are involved in the delivery of autophagic vesicles to the vacuole.

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Modulation of microtubule shape in vitro by high molecular weight microtubule associated proteins MAP1A, MAP1B, and MAP2

Cited by 18 publications

References 31 publications

The control of microtubule stability in vitro and in transfected cells by MAP1B and SCG10

The control of microtubule stability in vitro and in transfected cells by MAP1B and SCG10

Effects of NaCN and ionomycin on neuronal viability and on the abundance of microtubule-associated proteins MAP1, MAP2, and tau in isolated chick cortical neurons

Aut2p and Aut7p, two novel microtubule-associated proteins are essential for delivery of autophagic vesicles to the vacuole

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