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What You Will Learn in This Chapter In this chapter, instructors will develop foundational knowledge about how to select and use computational tools to teach CRISPR-Cas technologies. Broadly speaking, CRISPR-Cas is a sequence-based technology. Computational resources provide a platform for managing and interacting with these sequences. With appropriate instructional design, computational tools are a valuable complement to lessons about CRISPR-Cas technologies and are essential support tools for CRISPR-Cas experiments. With an ever-growing suite of computational tools available, in this chapter, instructors will learn to navigate the landscape of these tools to select the most appropriate tools for their classroom or laboratory needs. Instructors will learn to identify when computational resources are appropriate for use in their classroom (and when they are not appropriate), then how to select the most appropriate tools for their unique needs. Additionally, we introduce instructors to best practices in instructional design for using CRISPR-Cas computational tools in the classroom. Throughout, instructors will learn both the rationale and principle behind selection so they can evaluate tools discussed in this chapter and new ones as they become available. 

Proper heart morphogenesis requires a delicate balance between hemodynamic forces, myocardial activity, morphogen gradients, and epigenetic signaling, all of which are coupled with genetic regulatory networks. Recently both in vivo and in silico studies have tried to better understand hemodynamics at varying stages of veretebrate cardiogenesis. In particular, the intracardial hemodynamics during the onset of trabeculation is notably complex—the inertial and viscous fluid forces are approximately equal at this stage and small perturbations in morphology, scale, and steadiness of the flow can lead to significant changes in bulk flow structures, shear stress distributions, and chemical morphogen gradients. The immersed boundary method was used to numerically simulate fluid flow through simplified two-dimensional and stationary trabeculated ventricles of 72, 80, and 120 h post fertilization wild type zebrafish embryos and ErbB2-inhibited embryos at seven days post fertilization. A 2D idealized trabeculated ventricular model was also used to map the bifurcations in flow structure that occur as a result of the unsteadiness of flow, trabeculae height, and fluid scale ( R e ). Vortex formation occurred in intertrabecular regions for biologically relevant parameter spaces, wherein flow velocities increased. This indicates that trabecular morphology may alter intracardial flow patterns and hence ventricular shear stresses and morphogen gradients. A potential implication of this work is that the onset of vortical (disturbed) flows can upregulate Notch1 expression in endothelial cells in vivo and hence impacts chamber morphogenesis, valvulogenesis, and the formation of the trabeculae themselves. Our results also highlight the sensitivity of cardiac flow patterns to changes in morphology and blood rheology, motivating efforts to obtain spatially and temporally resolved chamber geometries and kinematics as well as the careful measurement of the embryonic blood rheology. The results also suggest that there may be significant changes in shear signalling due to morphological and mechanical variation across individuals and species.