Interkinetic nuclear migration (INM) is another interphase cell behavior that has been linked with neurogenesis (Baye and Link,2008; Taverna and Huttner,2010). INM is the process by which nuclei of neuroepithelial cells move in concert with progression through the cell cycle. M-phase nuclei are positioned at the apical-most region. G1/S-phase nuclei move to more basal locations. During G2 phase, nuclei rapidly move back to the apical surface to re-enter M-phase and undergo cytokinesis again (Fig 2). This phenomenon is conserved from mammals to Cnidaria and evidence suggests that cell-cycle progression is required for INM (Baye and Link,2008; Meyer et al.,2011). Both microtubule motors and actomyosin contraction play roles in nuclear movement, although the relative influences appear to vary between species and/or regions of the CNS (Del Bene et al.,2008; Norden et al.,2009; Tsai et al.,2010; Meyer et al.,2011; Kosodo et al.,2011). In addition to directed nuclear migration, there are also large non-autonomous effects where the movements and jostling of adjacent nuclei affect each other (Norden et al.,2009; Kosodo et al.,2011). The nuclear movements, therefore, are not completely stereotyped and the basal apex of the migration cycle is variable, fitting a normal distribution (Baye and Link,2007; Norden et al.,2009; Meyer et al.,2011; Kosodo et al.,2011). The first insights to a possible fate-influencing role for INM came from pharmacological manipulations to the cytoskeleton, which showed alterations to INM and affected neurogenesis (Murciano et al.,2002; Frade,2002). Potentially, such disturbances perturbed multiple parameters that affected neurogenesis. Significantly however, within zebrafish retinal neuroepithelial cells, the pattern of INM was found to correlate with neurogenesis (Baye and Link,2007). Specifically, cells with nuclei that moved more basally during interphase were highly biased to divide neurogenically in the next mitosis. In fact, the farther nuclei moved from the apical surface, the more likely the progenitor cell produced neurons in the next division. This relationship between nuclear position and neurogenesis was found to depend on apicobasal cell polarity and blocking neurogenesis did not change the patterns of nuclear migration (Baye and Link,2007). In a subsequent study, INM was assessed in a mutant for dynactin/p150, an activating subunit of cytoplasmic Dynein (Del Bene et al.,2008). Mutant cell nuclei were found to migrate more basally and neurogenesis was accelerated. Furthermore, computational analysis of imaged mouse retinal neuroepithelial cell behaviors in vitro revealed that one of the parameters that could be used to predict the mode of cell division was nuclear movements (Cohen et al.,2010). Overall, these results suggest that nuclear position during interphase influences the mode of cell division in the subsequent mitosis by responding to polarized signals within the cell (Fig. 6). Experimental perturbation of the developing mouse cortex also supports a role for INM in influencing neurogenesis. For example, in cortical progenitors, if microtubule coupling between the apical centrosome and the nucleus is disrupted, INM is impaired and the progenitor pool is depleted through excessive cell-cycle exit. Additional experiments that affected microtubule motors, interactions of motors with the nucleus, or actomyosin contraction also altered neurogenesis in mouse neural progenitors (Ge et al.,2010; Schenk et al.,2009; Tsai et al.,2005, 2009; Xie et al.,2007; Zhang et al.,2009). However, for the mouse cortex, time-lapse analysis to test whether the depth of nuclear movements correlate with the mode of cell division is lacking.