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A more recent version of this article appeared on April 1, 2004
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Submitted on September 17, 2003
Revised on December 22, 2003
Accepted on December 27, 2003
1 Max-Planck-Institut für terrestrische Mikrobiologie, Karl-von-Frisch-Stra
e, D-35043 Marburg, Germany, Hanulova 1, 84101 Bratislava, Slowakei
2 Max-Planck-Institut für terrestrische Mikrobiologie, Karl-von-Frisch-Strae, D-35043 Marburg, Germany
3 Max-Planck-Institut für terrestrische Mikrobiologie, Karl-von-Frisch-Strae, D-35043 Marburg, Germany, Institut für Zellbiologie, LMU, Schillerstr. 42, D-80336 München, Germany
* Corresponding author. E-mail address: Gero.Steinberg{at}staff.uni-marburg.de.
The microtubule cytoskeleton supports cellular morphogenesis and polar growth, but the underlying mechanisms are not understood. In a screen for morphology mutants defective in microtubule organization in the fungus Ustilago maydis we identified eca1 that encodes a sarcoplasmic/endoplasmic calcium ATPase (SERCA). Eca1 resides in the endoplasmic reticulum and restores growth of a yeast mutant defective in calcium homeostasis. Deletion of eca1 resulted in elevated cytosolic calcium levels and a severe growth and morphology defect. While F-Actin and myosin V distribution is unaffected, 
eca1 mutants contain longer and disorganized microtubules that show increased rescue and reduced catastrophe frequencies. Morphology can be restored by inhibition of Ca2+/CaM-dependent kinases or destabilizing microtubules, indicating that calcium-dependent alterations in dynamic instability are a major cause of the growth defect. Interestingly, dynein mutants show virtually identical changes in microtubule dynamics and dynein-dependent ER motility was drastically decreased in eca1. This indicates a connection between calcium signaling, dynein and microtubule organization in morphogenesis of Ustilago maydis.
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