## Abstract So far, there has been a discrepancy between the velocities of kinesin‐dependent microtubule motility measured __in vitro__ and within cells. By changing ATP, Mg^2+^, and kinesin concentrations, pH and ionic strength, we tried to find conditions that favour microtubule gliding across ki
MICROTUBULE FORMATION AND KINESIN-DRIVEN MICROTUBULE GLIDING IN VITRO IN THE PRESENCE OF LIPOPOLYSACCHARIDE
✍ Scribed by Konrad J Böhm; Stefan Russwurm; Nagib Ghaleb; Konrad Reinhart; Eberhard Unger
- Publisher
- Elsevier Science
- Year
- 1999
- Tongue
- English
- Weight
- 412 KB
- Volume
- 23
- Category
- Article
- ISSN
- 1065-6995
No coin nor oath required. For personal study only.
✦ Synopsis
Lipopolysaccharide (LPS) is a main trigger substance for the development of septic shock and multiple organ failure. We showed by turbidity measurements that LPS inhibits microtubule formation in a pH‐dependent manner. Inhibition was found to be not only due to sequestration of MAP2 by LPS, but also of MAP1 and tau MAPs, indicating that LPS is able to react with a broad variety of MAPs. LPS‐induced inhibition of microtubule formation could be compensated by additional tau or by addition of taxol. Dot blots revealed that LPS binds directly to tau, but seems not to bind to tubulin. As tau is expressed in various tissue types involved in multiorgan failure, it might be regarded as a further target for LPS action. In contrast, kinesin‐dependent microtubule gliding was not affected by LPS. The toxin neither blocked the cargo (vesicle) nor the microtubule binding site of kinesin, suggesting a certain specificity of LPS‐MAP interaction.
📜 SIMILAR VOLUMES
We studied the effect of alkaline-earth metal ions on the kinesin-driven gliding of microtubules, using a narrow glass chamber enabling the exchange of buffer components without interrupting microscopic observation. Under standard conditions (0.5 mM Mg 21 ), microtubules were found to glide at a mea