Cells rely heavily on their polarity establishment and maintenance mechanisms, because proper polarization is required for performing a wide range of cell functions. The unicellular ciliate Stentor is an excellent model system for studying polarity due to its giant size, extraordinary level of structural regularity of its cytoskeleton, and amenability to microsurgical manipulation. Importantly, Stentor has the capacity to regenerate any of its parts, which gives access to studying the re-establishment of polarity perturbed in a wide variety of ways. In this study, we used RNAi to analyze the role of Stentor cytoskeleton and molecular motors in cell motility, cell polarity, dynamic cell shape control, and regeneration. We show that cytoplasmic dyneins are essential for cell polarity maintenance, with abnormal cell morphologies observed when the corresponding genes are knocked down. We also observed that when kinesin gene is knocked down, Stentor cells are unable to extend to their full length. This suggests that kinesin may be involved in the sliding of microtubule sheets within microtubule rows running parallel to the main axis of the cell. Sliding within this complex cytoskeletal structure is thought to provide the mechanistic basis for Stentor dynamic shape changes. In addition to cytoplasmic dyneins and kinesin, we uncovered B subunit of the protein phosphatase PP2A as a major player in Stentor morphology control. Thus, our results provide insights into the molecular basis of Stentor morphology maintenance and dynamic cell shape control. Better molecular understanding of Stentor amazing ability to regenerate is essential, because it may lead to advancements in regenerative medicine..