Correct nuclear position is crucial for cellular function. The cytoskeletal mechanisms of nuclear positioning have been studied intensely in cultured cells. However, it is less clear if and how tissue morphology can influence nuclear positioning in developing tissues. To address this question, this thesis compares nuclear migration in straight and curved neuroepithelia of the developing zebrafish. Neuroepithelial nuclei occupy different apicobasal positions in interphase but migrate to the apical surface before mitosis, a process essential for epithelial development. While apical migration in the straight hindbrain and the curved retina depends on actomyosin, it is unclear how the necessary forces are generated and if tissue morphology influences the force generation mechanisms. Remarkably, this study demonstrates that in neuroepithelia of different shape nuclei move with distinct kinetics and undergo distinct deformations. Such differences are explained by the action of disparate forces that propel hindbrain and retinal nuclei. In agreement with this conclusion, hindbrain and retinal cells display distinct actomyosin distribution and regulation during nuclear migration. Apical movement is shown to depend on Rho-ROCK activity in the hindbrain and formin activity in the retina. Therefore, hindbrain and retinal cells employ distinct actin-dependent mechanisms of nuclear positioning. Comparison of nuclear movements in another pair of straight and curved neuroepithelia shows that in tissues with similar morphology nuclei have conserved modes of apical migration. The different mechanisms of apical migration used in tissues of different shape argue that tissue morphology can indeed influence the mechanism of nuclear positioning. The findings in this thesis suggest that different mechanisms arise due to differences in actin arrangements during development of tissues with distinct curvature. Furthermore, they emphasize the importance of developmental context, tissue and cell morphology for the execution of intracellular processes.:1. INTRODUCTION 1.1. The cytoskeleton is a versatile tool to perform a variety of cellular functions 1.1.1. Introduction to microtubules and actomyosin 1.1.2. Functions of the cytoskeleton 1.1.3. The cytoskeleton and intracellular transport 1.2. The cytoskeleton in nuclear positioning 1.2.1. The nucleus can be coupled to the cytoskeleton 1.2.2. Mechanisms of nuclear positioning by microtubules and actin 1.2.3. Nuclear positioning in the pseudostratified epithelium 1.3. Objective of the study 2. MATERIALS AND METHODS 2.1. Zebrafish methods 2.1.1. Zebrafish husbandry 2.1.2. RNA and DNA injections 2.1.3. Cloning strategies 2.1.4. List of constructs 2.1.5. Heat shock of embryos 2.1.6. Drug treatments 2.1.7. Immunofluorescence 2.2. Image acquisition 2.2.1. Confocal scans 2.2.2. Time-lapse imaging using spinning disk confocal microscope (SDCM) 2.2.3. Time-lapse imaging using light-sheet fluorescent microscope (LSFM) 2.3. Laser ablations 2.3.1. PSE laser ablations 2.3.2. Nuclear laser ablations 2.4. Image analysis 2.4.1. Sample drift correction 2.4.2. Actin, myosin, and nuclear intensity distribution 2.4.3. Nuclear segmentation, shape measurements, and tracking in 3D 2.4.4. Analysis of the kinetics of apical nuclear migration 2.4.5. Tissue and cell shape measurements 3. RESULTS 3.1. Characterization of apical nuclear migration in zebrafish neuroepithelia 3.1.1. The overall duration of G2 and apical migration differ in hindbrain and retina 3.1.2. Hindbrain and retinal nuclei move with distinct kinetics during apical migration 3.2. Nuclear deformations can be used to study the forces experienced by the organelle 3.2.1. The absence of lamin A/C is likely to enable nuclear deformations 3.2.2. Neuroepithelial nuclei can respond to applied forces by deformation 3.2.3. Retinal nuclei deform more strongly during apical migration 3.2.4. Deformation of ablated regions in the nucleus suggests that retinal nuclei are pushed to the apical side 3.3. Apical nuclear migration depends on actomyosin with distinct distribution in hindbrain and retina 3.3.1. Apical nuclear migration in the hindbrain depends on actin and not on microtubules 3.3.2. Actin and myosin are locally enriched basally of the nucleus in retinal cells but not in hindbrain G2 cells 3.4. Apical nuclear migration is regulated differently in hindbrain and retinal cells 3.4.1. Initial screening for possible actomyosin regulators of apical nuclear migration 3.4.2. Apical nuclear migration is controlled by different actomyosin regulators in hindbrain and retinal cells 3.5. Cells of neuroepithelia with distinct curvature use different mechanisms of apical migration 3.5.1. Tissue-wide contractile actomyosin that is enriched basally in the retina, is absent in the hindbrain 3.5.2. Tissue curvature and cell shape differ between hindbrain and retina 3.5.3. Characterization of the straight and the curved regions of the MHB 3.5.4. Nuclei in straight and curved neuroepithelia move with distinct kinetics 3.5.5. Nuclear shape changes during apical migration are stronger in curved compared to straight neuroepithelia 3.5.6. Basal cytoplasmic actomyosin follows the nucleus in cells of curved neuroepithelia 4. DISCUSSION 4.1. The deformability of neuroepithelial nuclei as a prerequisite for migration in the crowded PSE 4.2. Possible mechanisms of apical nuclear migration 4.2.1. Cortical flow-dependent mechanism in the hindbrain 4.2.2. Basal pushing mechanism in the retina 4.2.2.a. Pushing of the nucleus by a cytoplasmic flow 4.2.2.b. Pushing of the nucleus by an expanding actin network 4.2.2.c. Possible roles of myosin in a basal pushing mechanism 4.3. The adaptability of the cytoskeleton ensures robust apical nuclear migration 4.3.1. Cytoskeleton adaptability ensures the robustness of apical nuclear migration 4.3.2. Adaptation of the actomyosin cytoskeleton to different tissue curvature 5. OUTLOOK LIST OF ABBREVIATIONS LIST OF TABLES LIST OF FIGURES MOVIE LEGENDS REFERENCES APPENDIX