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Gaspar, I., Szabad, J. (2009). Glu415 in the {alpha}-tubulins plays a key role in stabilizing the microtubule-ADP-kinesin complexes.  J. Cell Sci. 122(16): 2857--2865.
FlyBase ID
FBrf0208585
Publication Type
Research paper
Abstract

Kavar(21g), a dominant female-sterile mutation of Drosophila, identifies the alphaTubulin67C gene that encodes alpha4-tubulin, the maternally provided alpha-tubulin isoform. Although alpha4-tubulin is synthesized during oogenesis, its function is required only in the early cleavage embryos. However, once present in the developing oocyte, much of the alpha4-tubulin and the Kavar(21g)-encoded E426K-alpha4-tubulin molecules become incorporated into the microtubules. We analyzed ooplasmic streaming and lipid-droplet transport, with confocal reflection microscopy, in the developing egg primordia in the presence and absence of alpha4-tubulin and E426K-alpha4-tubulin and learnt that the E426K-alpha4-tubulin molecules eliminate ooplasmic streaming and alter lipid-droplet transport. Apparently, Glu426 is involved in stabilization of the microtubule-kinesin complexes when the kinesins are in the most labile, ADP-bound state. Replacement of Glu426 by Lys results in frequent detachments of the kinesins from the microtubules leading to reduced transport efficiency and death of the embryos derived from the Kavar(21g)-carrying females. Glu426 is a component of the twelfth alpha-helix, which is the landing and binding platform for the mechanoenzymes. Since the twelfth alpha-helix is highly conserved in the alpha-tubulin family, Glu415, which corresponds to Glu426 in the constitutively expressed alpha-tubulins, seems be a key component of microtubule-kinesin interaction and thus the microtubule-based transport.

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    J. Cell Sci.
    Title
    Journal of Cell Science
    Publication Year
    1966-
    ISBN/ISSN
    0021-9533
    Data From Reference
    Aberrations (3)
    Alleles (7)
    Genes (7)
    Insertions (1)